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Microbiology 2125 > Unit 5-Immunology+Viruses > Flashcards

Unit 5-Immunology+Viruses Flashcards

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1
Q

Eosinophils

A

Eosinophils are a type of disease-fighting white blood cell. This condition most often indicates a parasitic infection, an allergic reaction or cancer.

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2
Q

Immune Response Design functions

A

• surveillance surveillance • recognition recognition • attack attack • destruction destruction • proportional response

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3
Q

Levels of Defense

A

First Second Third

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4
Q

First Line of Defense

A

Non-specific Barrier Defenses Body Excretions (Tears, Sweat)

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5
Q

Second line of defense

A

Non-Specific Inflammation Couplement (antimicrobial proteins) Phagocytosis

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6
Q

Third Line of defense

A

Specific And adaptive Antibodies (antimicrobial proteins) Cytotoxic Cells

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7
Q

Levels of defense Timing

A

Primary (first encounter) Secondary (subsequent encounters)

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8
Q

Non-Specific Host Defenses

A

Intact Skin (Stratum Corneum) Mucous membranes Responses (Typically involve secretions)

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9
Q

Mechanical Host Defense responses

A

Mechanical • tears • saliva • ciliary action • vomiting • urination • coughing • sneezing

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10
Q

Chemical Host Defense Responses

A

lysozyme • sweat/oils • dermcidin • hydrochloric acid

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11
Q

Lysozyme

A

an enzyme that catalyzes the destruction of the cell walls of certain bacteria, occurring notably in tears and egg white

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12
Q

Dermcidin

A

an antimicrobial peptide secreted by sweat glands that attacks any bacteria on our skin

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13
Q

Inflammation

A

Increased blood flow to the affected area (arterioles constrict) Edema Phagocytosis by immune response cells Fever Completment activated Chemical signaling

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14
Q

Phagocytosis

A

the ingestion of bacteria or other material by phagocytes and amoeboid protozoans.

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15
Q

Pyrogens

A

a substance, typically produced by a bacterium, that produces fever when introduced or released into the blood.

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16
Q

Pluripotent stem cells can turn into what type of cells?

A

Erythrocytes Leukocytes Platelets

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17
Q

Components of blood

A

Platelets Erythrocytes Leukocytes Plasma

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18
Q

Two types of Leukocytes

A

Granular (Lobed Nucleus) Agranular (Round Nucleus)

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19
Q

Granular Leukocytes can turn into what type of cells?

A

Basophils Neutrophils Eosinophils

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20
Q

Basophils

A

Few in #, secrete Histamine, triggering inflammation

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21
Q

Neutrophils

A

A Majority in #, short-lived (A few days), found mostly in tissues and function in phagocytosis

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22
Q

Eosinophils

A

Few in #, directed against large, multicellular parasites; function in inflammation

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23
Q

Agranular Leukocytes can turn into what kind of cells?

A

Monocytes Lymphocytes

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24
Q

Monocytes

A

Third most common in number, function in phagocytosis

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25
Q

Lymphocytes

A

Second most common, secrete antibodies and destroy infected cells.

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26
Q

Monocytes can turn into what type of cells?

A

Macrophages

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27
Q

Macrophage

A

a large phagocytic cell found in stationary form in the tissues or as a mobile white blood cell, especially at sites of infection.

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28
Q

Lymphocytes turn into what type of cells?

A

B-Cell T-Cell

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29
Q

Antigen

A

a toxin or other foreign substance that induces an immune response in the body, especially the production of antibodies.

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30
Q

What cells are antigen-presenting cells

A

Macrophages

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31
Q

Humoral response

A

involves B cells that recognize antigens or pathogens that are circulating in the lymph or blood

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32
Q

Cell-Mediated Response

A

an immune response that does not involve antibodies, but rather involves the activation of phagocytes, antigen-specific cytotoxic T-lymphocytes, and the release of various cytokines in response to an antigen

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33
Q

What type of cells generate Plasma Cells?

A

B-Lymphocytes

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34
Q

what type of cells generate Cytotoxic T-Cells?

A

T-Lymphocytes

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35
Q

What type of cells generate Antibodies?

A

Plasma Cells

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36
Q

Function of Antibodies in the Immune Repsonse Cascade

A

Signals phagocytic cells and activates complement (Extracellularly located pathogens)

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37
Q

Function of Cytotoxic T-Cells

A

Destroy the body’s own infected cells (Intracellularly located pathogen)

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38
Q

secondary immune response in the cascade

A

Antigen causes memory B or T Cell activation, generating Plasma or Cytotoxic T-cells.

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39
Q

Antigen recognition and Clonal Selection

A

Using genetic recombination, the body produces many different cell-surface proteins capable of recognizing many different antigens

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40
Q

when an antigen appears, it will bind to its B or T Cell w/ the matching receptor. Then what happens?

A

The cell will be induced to divide to create additional copies of the cell.

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41
Q

Antibodies

A

glycoproteins (Combinations of Amino Acid Chains and sugars) that can be found in the blood serum (Soluble Antibodies) or attached to the surface of certain cells such as B-Lymphocytes

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42
Q

Antibody Structure

A

four separate polypeptide chains held together by disulfide bridges. Two are longer/larger (Heavy chains) and are identical to one another. And 2 light chains (Smaller) w their own variable and constant regions

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43
Q

Antibody Domain structure

A

Variable domain constant domain Hinge Constant Domain 2 Constant Domain 3

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44
Q

Paratope

A

Antigen-Binding Site

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45
Q

Binding of an antigen occurs

A

On the Epitope (on the antigen) and the Paratope (On the Antibody)

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46
Q

What are the 5 types of Antibodies

A

IgG IgD IgA IgM IgE

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47
Q

IgG

A

Single Monomer Triggers/activates complement proteins May enter tissue fluids can cross the placenta to protect the fetus

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48
Q

What is the most abundant class of Antibody?

A

IgG (80%)

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49
Q

IgA comprises what % of antibodies

A

10-15%

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50
Q

IgA structure

A

Dimeric (2 Y-shaped w the usual 2 heavy and light chains)

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51
Q

IgA

A

Found in Body secretions (Saliva, tears, perspiration, breast milk) Bind to pathogen/antigen to prevent adhesion to body surfaces

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52
Q

IgD

A

Single Monomer Located on the cells of B-Lymphocytes Function as Antigen receptors May bind to basophils/mast cells stimulating inflammation

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53
Q

IgE

A

Single Monomer Can interact w Basophils (In bloodstream) and mast cells (In connective tissue) to release histamine and other chemical signals Generates an inflammatory response

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54
Q

IgM

A

First to appear in the infection process 10-15% of antibodies 5 Y-Structures joined around a common center (Pentameric) Functions in agglutination and complement function

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55
Q

Zymogen

A

an inactive substance that is converted into an enzyme when activated by another enzyme

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56
Q

Proper immune system functioning depends on

A

Proportional responses to the offending agents

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57
Q

Immunodeficiency can lead to

A

Cancers

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58
Q

Autoimmunity can lead to

A

Hypersensitivities (Lupus, RA, Psoriasis)

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59
Q

Autoimmunity

A

the system of immune responses of an organism against its own healthy cells and tissues. Any disease that results from such an aberrant immune response is termed an “autoimmune disease”.

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60
Q

Passive Immunity

A

the short-term immunity that results from the introduction of antibodies from another person or animal.

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61
Q

Active Immunity

A

the immunity that results from the production of antibodies by the immune system in response to the presence of an antigen

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62
Q

Natural (Innate) Immunity

A

the inborn ability of the body to protect itself against pathogens and is transferred from mother to the baby.

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63
Q

Artificial Immunity

A

can be induced by a vaccine, a substance that contains antigen. A vaccine stimulates a primary response against the antigen without causing symptoms of the disease.

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64
Q

The Antibiotic Discovery Void began when?

A

around 1990

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65
Q

Staphylococcus Characteristics

A

Gram (+) Cocci No flagellae No endospores Capsules Facultative Anaerobe Common in the environment (Soil Microbe), Harbored by humans intermittently Resistant to many physical extremes

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66
Q

Facultative Anaerobe

A

an organism that makes ATP by aerobic respiration if oxygen is present, but is capable of switching to fermentation or anaerobic respiration if oxygen is absent

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67
Q

Obligate Anaerobe

A

poisoned by oxygen, so they gather at the bottom of the tube where the oxygen concentration is lowest

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68
Q

What types of Exotoxins to Staphylococcus produce?

A

Coagulase Hyaluronidase Hemolysins Leukocidins enterotoxins Exfoliative Toxins

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69
Q

How does Staphylococcus usually enter the body

A

Typically through hair follicles or wounds (cutaneous)

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70
Q

Some strains of Staphylococcus aureus may be resistant

A

MRSA (Multiple Resistant Staphylococcus Aureus) or Penicillinase resistance

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71
Q

MRSA is resistant to what drugs?

A

Methicillin Oxacillin Penicillin Amoxicillin

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72
Q

Staphylococcus infections typically produce what skin lesions?

A

Furuncles and Carbuncles

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73
Q

Systemic Staphylococcus infections typically result in

A

Bacteremia or Sepsis

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74
Q

Systemic infections from staphylococcus can spread and cause

A

Osteomyelitis Meningitis Pneumonia

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75
Q

Staphylococcus is cultured on what type of Agar?

A

SBA (Sheep’s Blood Agar) or MSA (Mannitol Salt Agar)

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76
Q

Common Staphylococcus Species

A

S. Aureus S. Capitis S. Epidermidis S. Hominis S. Saprophyticus

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77
Q

Staphylococcal skin lesions

A

Carbuncle/Furuncle Imetigo Styes Scalded Skin Syndrome

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78
Q

Staphylococcal Food poisoning

A

usually caused by contaminated milks and cheeses Salt Tolerant Heat Resistant Sliced Meat, Pudding, pastries, sandwiches

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79
Q

Symptoms of Staphylococcal Food Poisoning?

A

nausea, vomiting, stomach cramps, diarrhea

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80
Q

Streptococcus characterisics

A

Gram (+) Cocci No Flagellae No Endospores May posess capsule+ Slime Layers Facultative Anaerobe

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81
Q

True or False: Streptococci are hearty bacteria which are not very sensitive to the environment?

A

False: They are susceptible to environmental factors 9Drying, heat, disinfectants)

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82
Q

What is an important part of classification of Streptococcal bacteria?

A

Hemolysis (Alpha, Beta, Gamma)

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83
Q

Alpha hemolysis

A

Partial Degredation of RBCs

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84
Q

Beta Hemolysis

A

Complete degredation/rupture of RBCs

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85
Q

Gamma Hemolysis

A

No Degredation of RBCs

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86
Q

Streptolysins

A

SL-O and SL-S Damage cells other than RBCs

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87
Q

Common Streptococcal species

A

S. Agalactiae S. Faecalis S. Pneumoniae

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88
Q

Streptococcus pneumoniae

A

causative agent of most bacterial pneumonias (encapsulated w Polysaccharide layer for enhanced virulence) can also cause meningitis and otitis media

89
Q

Streptococcus Pyogenes

A

Most pathogenic Humans are reservoir gnetic highly variable

90
Q

Streptococcus pyogenes virulence factors

A

polysaccharides tolerate lysozyme lupotechoic acids on fimbriae M-Proteins Streptolysins (exotoxin) Streptokinase(Penetrate host tissue) c5a Protease (Inactivates neutrophil response)

91
Q

Streptococcus Mutans

A

Plays a significant role in tooth decay creates biofilm on tooth enamel metabolizes various carbohydrates producing lactic acid as a byproduct

92
Q

Clostridium

A

Gram (+) Bacilli No flagellae produce endospores obligate Anaerobe Saprophytic

93
Q

Saprophytic

A

an organism which gets its energy from dead and decaying organic matter

94
Q

Disease-Causing Clostridium species in humans

A

C. Tetani C. botulinum C. Difficile C. Perfringens

95
Q

Gas Gangrene

A

When bacteria or spores enter the wound where the blood supply is interrupted, anaerobic state arises and allows bacteria to multiply and leads to necrosis. Bacterium releases carbon dioxide and hydrogen gas causing the tissue to swell and inflate/ Effective treatment involves Debridement (C. Perfringens)

96
Q

Antibiotic-Associated Disease

A

Clostridium Difficile

97
Q

Tetanus

A

A serious bacterial infection that causes painful muscle spasms and can lead to death.

98
Q

Clostridium Tetani

A

Gram (+) bacillus Obligate Anaerobe Spore-Forming Present in contaminated soil from fecal waste Produces Tetanus Neurotoxin

99
Q

Tetanus Neurotoxin (TeNT)

A

Prevents neurons from releasing certain neurotransmitters that inhibit muscle contraction so muscles remain in a permanently contracted state

100
Q

True or False: The binding of TeNT is reversible

A

False: It is irreversible

101
Q

Tetanus structure

A

Composed of 2 protein chains (heavy and light)

102
Q

True or False: The Toxoid vaccination for Tetanus does not give lifelong immunity

A

True: Booster shots are required every ten years or so

103
Q

True or False: The amount of TeNT that can be fatal causes the response ot be immunogenic

A

False: It is too low to be immunogenic. Exposure to the toxin does not elicit an immune response while still being fatal

104
Q

Botulism

A

clostridium Botulinum Common in soil and water Produces Botulinum toxin under certain growth conditions Endospores will germinate and grow, producing the toxin in certain conditions requires a bacteriophage infection

105
Q

How does the botulinum toxin work

A

Prevents acetyl choline release at neuromuscular Junctions (NMJ), resulting in flaccid paralysis

106
Q

Forms of Botulinum toxin

A

Foodborne, Infant (Colonization of the gut) and wound

107
Q

Can the botulinum toxin be destroyed?

A

Yes, by heating ot the proper temperature for a certain period of time

108
Q

Symptoms of a botulinum toxin infection

A

blurred vision, drooping eyelids, loss of facial expression, paralysis progressing from head and neck to chest and legs

109
Q

Is there an effective antitoxin available for botulinum toxin?

A

Yes

110
Q

Bacillus Anthraxis

A

Gram (+) Bacillus Obligate Anaerobe Spore-Forming organism w spores viable for decades

111
Q

Exotoxins formed by Bacillus Anthracis

A

Protective Antigen ( Allows toxins to enter cells) Edema Factor Lethal Factor

112
Q

Forms of Anthrax (Based on Exposure route)

A

Cutaneous Gastrointestinal inhalational

113
Q

Cutaneous Anthrax

A

Spores enter through breaks in the skin, forms popular-vesicular lesions, low mortality if antibiotics are used

114
Q

Gastrointestinal Anthrax

A

spores are ingested, 50% mortality if left untreated

115
Q

Inhalational Anthrax

A

Spores drawn into the lungs. Most dangerous form. near 100% mortality if left untreated

116
Q

Borrelia burgdorferi

A

Spirochete Bacteria (Gram does not apply) Causes Lyme Disease

117
Q

Lyme Disease

A

Caused by Borrelia burgdorferi Zoonotic Disease Transmitted by Ixodes, Ticks (2-3 Days required)

118
Q

Lyme Disease Reservoir

A

Field Mice

119
Q

Lyme Disease Symptoms

A

Fatigue, Chills, Fever, Headache, Muscle/Joint Pain Distinctive rash (Erythema migrans (TARGET)

120
Q

Francisella Tularensis

A

Causes Tulaermia Gram (-) Cocci-Bacillus

121
Q

Tularemia

A

Caused by Francisella tularensis Zoonotic disease highly infectius

122
Q

Tularemia Reservoir

A

Rabbits/hares, Rodents

123
Q

Tularemia Vector

A

Ticks

124
Q

Tularemia Symptoms

A

Fever, Chills, headaches, diarrhea, muscle aches, joint pain

125
Q

Tularemia infection routes

A

Skin (Animal Bites) (Ulceration may occur) Eye (Conjuctiva) Mouth (Contaminated food/water) Lungs (inhaled dust/aerosols, coughing, chest pain and difficulty breathing

126
Q

Mycobacterium Tuberculosis

A

Acid-Fast Bacillus (Mycolic acids in cell wall) Obligate Anaerobe Resistant to drying, disinfectants, and antibiotics

127
Q

Tuberculosis

A

caused by Mycobacterium tuberculosis Slow Growing Long courses of antibiotics for treatment acquired through inhalation and close extended contact

128
Q

Fish tank Granuloma

A

Caused by Mycobacterium Marinum

129
Q

Leprosy/Hansen’s Disease

A

caused by Mycobacterium Leprae

130
Q

Diptheria

A

Caused by Corynebacterium diptheriae Spread by aerosol droplets (cough or sneeze)

131
Q

Corynebacterium diptheriae

A

Gram (+) Bacillus Obligate Anaerobe Causes Diptheria No flagella or endospores Found in soil and water Bacteriophage allows it to produce homodimer (exotoxin)

132
Q

How does Corynebacterium diptheriae damage the host cells

A

Interfering with protein synthesis

133
Q

Sequelae of Diptheria

A

Myocarditis and neuropathy

134
Q

Untreated Mortality rate of diptheria

A

50%

135
Q

treated Mortality rate of diptheria

A

10%

136
Q

There is no vaccine for Diptheria

A

FALSE (tDAP)

137
Q

Listeria

A

Gram (+) Bacilli Facultative anaerobe No Spores Produce flagellae @ low temps Grows between 39-100 F Found in soil and water through animal fecal waste

138
Q

What bacterium causes Listeria

A

Listeria Monocytogenes

139
Q

What patient population is affected by Listeria?

A

Children, Pregnant women, and immunocompromised patients (elderly, cancer, immunosuppressed)

140
Q

Upon infection, How does listeria spread

A

Spreads to the bloodstream, causing sepsis or to the central nervous system (causing meningitis - 50% mortality)

141
Q

True or False: Listeria can cross the placenta

A

True: Can lead to brain damage or death of the fetus

142
Q

Two pathogenic species of Nisseria in humans

A

Nisseria Gonorrhoeae Nisseria Meningitidis

143
Q

Nisseria

A

Gram (-) Diplococci Can resist phagocytic neutrophils complement proteins aren’t as effective

144
Q

Nisseria Meningitidis can produce a capsule, which does what in the body?

A

Protects it against antimicrobial proteins in the blood serum.

145
Q

Meningicoccal disease is most common where?

A

In group settings, among adolescents and young adults (colleges)

146
Q

How much of the population are carriers of Nisseria

A

10%

147
Q

How is Nisseria Meningitidis

A

Spread by respiratory droplets/ throat secretions/ saliva

148
Q

Nisseria Menengitidis symptoms

A

Inflammation of tissues surrounding the brain and can quickly prove fatal (non-fatal cases can result in life-long brain damage or hearing loss) May cause septicemia (Blood vessels are damaged and hemorrhage)

149
Q

Nisseria Meningitidis antibiotic resistance

A

Antibiotics can be effective if begun early enough. Effective Vaccine is available

150
Q

Yersinia Pestis

A

Plague

151
Q

Yersinia Pestis

A

Gram (-) Cocco-Bacillus Facultative anaerobe Host several virulence plasmids

152
Q

Yersinia Pestis Reservoir

A

Rodents (wild) and rats in urban settings

153
Q

Transmitting Vector of Yersinia Pestis

A

Fleas

154
Q

3 forms of Yersinia Pestis (Plague)

A

bubonic Septicemic Pneuomonic

155
Q

Bubonic Plague

A

Muscle aches, fever, weakness, tissue necrosis, lymphadenopathy (Bubose)

156
Q

Septicemic Plague

A

Fever, vomiting, nausea, abdominal pain, bleeding into tissues

157
Q

Pneumonic plague

A

fever, headache, weakness, chest pain+cough w/ blood, transmitted through respiratory droplets

158
Q

Is antibiotic treatment effective in Plage forms?

A

Yes, if it is started early enough

159
Q

Nucleocapsid

A

Nucleic acid and Capsid in a virus

160
Q

Capsid

A

Protein shell in a virus

161
Q

Naked Virus

A

Injects its nucleic acid from the outside of the host cell

162
Q

Encapsulated/enveloped virus

A

is engulfed into the cell in order to inject its nucleic acid

163
Q

Pleomorphic Viron

A

Has the ability to change its shape based on its environmental selective pressures

164
Q

Capsomere

A

a subunit of the capsid, an outer covering of protein that protects the genetic material of a virus. Capsomeres self-assemble to form the capsid

165
Q

Complex Virus

A

Contains additional virulence factors and protein filaments: fibrillar outer matrix, lip polysaccharides as well as the tail fibers, pins, collar and sheath of bacteriophages

166
Q

ssRNA

A

+ -

167
Q

ssRNA Virus

A

+ -

168
Q

Adsorption

A

host range determined by the ability of glycoproteins on host cell membrane receptors to bind to virion

169
Q

Penetration

A

through endocytosis or cell membrane fusion

170
Q

Uncoating

A

removal of envelope and capsid

171
Q

Synthesis

A

replication and translation of viral nucleic acid

172
Q

Assembly

A

viral proteins associate to create new capsids

173
Q

Release

A

cell lysis for non-enveloped, complex virions and budding or exocytosis for enveloped virions

174
Q

Steps of a Viral infection

A

Adsorption Penetration Uncoating Synthesis Assembly Release

175
Q

Cytopathic Changes in a host cell

A

Giant/Multinucleate Cells/Syncytial Clumping Cell Inclusions Genetic (Oncogenic Changes)

176
Q

Oncogenic changes

A

cells are transformed and are unable to regulate their own division

177
Q

Cell Inclusions

A

partially formed, crystalline capsids

178
Q

Origin of the Human Immunodeficiency Virus (HIV)

A

It is thought to have mutated from SIV (a retrovirus of the genus Lentivirus (species Simian immunodeficiency virus) that causes a disease in monkeys similar to AIDS and that is closely related to HIV-2 of humans — called also simian immunodeficiency virus ) and arose in the 1980s in San Francisco, CA

179
Q

Prion

A

A Misshapen infectious protein that promotes others to mutate

180
Q

Viruses can live and reproduce on their own outside the cell (T/F)

A

False: They are obligate intracellular parasites and are metabolically inert outside the cell.

181
Q

Simple Viruses

A

Nucleocapsid Only

182
Q

Complex virus

A

Nucleocapsid+ spikes, tails, pins, or fibrillar matirices

183
Q

What bodily fluids have high numbers of the HIV viron present?

A

Semen, Blood, Vaginal secretions, breast milk

184
Q

What bodily fluids have low numbers of the HIV Viron present?

A

Swear, Urine, tears, Saliva

185
Q

Rabies Virus structure

A

Enveloped, Single-Stranded, Non-Segmented RNA Virus

186
Q

How does the Rabies virus move through the body?

A

moves from peripheral nervous system to central nervous system and then migrates to salivary glands

187
Q

Initial symptoms of Rabies infection

A

fever, nausea, vomiting, headache and fatigue

188
Q

Manifestations of Rabies infection

A

“furious” (muscle spasm, seizures, pain swallowing) and “dumb” (disorientation and paralysis) with either one eventually leading to coma and death

189
Q

Treatments for Rabies

A

thorough wound cleaning, administered antibodies and a (intramuscular) vaccine (injection series)

190
Q

Opsonization (Antibody Function)

A

enhance macrophage attachment and phagocytosis

191
Q

agglutination (Antibody Function)

A

whole cells) / precipitation (soluble antigens -clumping of particles

192
Q

Complement Fixation (Antibody Function)

A

initiated by IgG and IgM that recruit complement proteins to form a membrane attack complex resulting in bacterial cell lysis

193
Q

Neutralization (Antibody Function)

A

prevent antigen from normal binding

194
Q

Four Primary ways Antibodies Function

A

Neutralization

agglutination

Complement Fixation

Opsonization

195
Q
A
196
Q

Describe the Infection/Lesion/Disease

A

Anthrax

197
Q

Identify the type of organisms present on the Bacterial Cell

A

Bacteriophage

198
Q

Identify the Lesion/Infection/Disease

A

Botulism

199
Q

Identify the Disease present in this patient

A

Colostrim Difficile (C. Diff)

200
Q

Identify the Infection/Lesion/Disease

A

Diptheria

201
Q

Identify the Infection/Lesion/Disease

A

Fish tank Granuloma

202
Q

Identify the Lesion/Infection/disease

A

Gas Gangrene

203
Q

Identify the Infection/Lesion/Disease

A

Hansen’s Disease/Leprosy

204
Q

Identify the Infection/Lesion/Disease

A

HIV

205
Q

Identify the Infection/Lesion/Disease

A

Listeria

206
Q

Identify the Infection/Lesion/Disease

A

Lyme disease

207
Q

Identify the Infection/Lesion/Disease

A

Lyme Disease

208
Q

Identify the Infection/Lesion/Disease

A

Measles

209
Q

Identify the Cell type

A

Multinucleate/Syncitial

210
Q

Identify the Infection/Lesion/Disease

A

Necrotizing Fasciitis

211
Q

Identify the cell structure present (arrows)

A

Negri Bodies

212
Q

Identify the Cell Type

A

Nisseria (Diplococci)

213
Q

Identify the Infection/Lesion/Disease

A

Plague (Black Plague)

214
Q

Identify the Infection/Lesion/Disease

A

Rabies

215
Q

Identify the Infection/Lesion/Disease

A

Rheumatic fever

216
Q

Identify the Infection/Lesion/Disease

A

Tetanus

217
Q

Identify the Infection/Lesion/Disease

A

Tuberculosis

218
Q

Identify the Infection/Lesion/Disease

A

Tuberculosis

219
Q

Identify the Infection/Lesion/Disease

A

Tullaremia

Microbiology 2125 (6 decks)

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