Micro Exam III

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Last updated 8:01 PM on 7/7/26
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149 Terms

1
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What are the three lines of host defense?

First line: physical/chemical barriers. Second line: innate internal defenses (inflammation, phagocytosis, fever, antimicrobial proteins). Third line: adaptive/acquired immunity.

2
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What characterizes the first line of defense?

Any barrier that blocks invasion at the portal of entry; nonspecific and very general in action.

3
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What characterizes the second line of defense?

An internalized system of protective cells and fluids (inflammation, phagocytosis) that acts rapidly, locally and systemically, once the first line is overcome.

4
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What characterizes the third line of defense?

Acquired individually as lymphocytes encounter each foreign substance; produces unique protective substances and provides long-term immunity.

5
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Define immunology.

The study of the body's second and third lines of defense, its response to infectious agents, and the study of allergies and cancer.

6
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What is the mandate of a healthy immune system?

Surveillance of the body, recognition of foreign material, and destruction of entities deemed foreign.

7
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What is an antigen (marker)?

A surface molecule (protein and/or sugar) that lets immune cells evaluate a cell as self and mark it for destruction if needed.

8
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What are PAMPs?

Pathogen-associated molecular patterns — markers shared by many different kinds of microbes.

9
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What are PRRs?

Pattern recognition receptors — used by host cells of the innate (2nd line) immune system to recognize PAMPs.

10
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What is the mononuclear phagocyte system (MPS)?

A network of phagocytic cells enmeshed in connective tissue reticulum, in direct contact with tissue cells and extracellular fluid.

11
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Name the primary lymphatic organs.

Red bone marrow and the thymus — sites of immune cell birth and maturation.

12
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Name the secondary lymphatic organs.

Lymph nodes, spleen, and associated lymphoid tissues — sites of immune cell activation, residence, and function.

13
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Where do B cells mature? Where do T cells mature?

B cells mature in the bone marrow; T cells mature in the thymus.

14
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What is the function of the spleen?

Filters blood (not lymph); removes worn-out red blood cells; filters pathogens for phagocytosis by macrophages; stores blood.

15
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What are SALT and MALT?

Skin-associated lymphoid tissue and mucosa-associated lymphoid tissue — diffuse bundles of lymphocytes beneath the skin/mucosa.

16
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What is GALT and what does it include?

Gut-associated lymphoid tissue; includes the appendix, lacteals, and Peyer's patches.

17
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Differentiate plasma and serum.

Plasma is the clear, yellowish fluid portion of whole blood; serum is the same fluid minus clotting factors (obtained from clotted blood).

18
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What are cytokines?

Small active molecules secreted by immune and other cells to regulate, stimulate, suppress, or otherwise control cell development, inflammation, and immunity.

19
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Give an example of a pro-inflammatory and an anti-inflammatory cytokine.

Pro-inflammatory: IL-1 or TNF-β. Anti-inflammatory: IL-10.

20
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Name the three types of phagocytes.

Neutrophils, monocytes, and macrophages.

21
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How do neutrophils differ from macrophages?

Neutrophils are general-purpose, early-responding phagocytes and the main component of pus; monocytes migrate into tissue and transform into long-lived macrophages.

22
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List the steps of phagocytosis in order.

Chemotaxis → adhesion → engulfment/phagosome formation → phagolysosome formation & killing → elimination (excretion of debris).

23
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What are histiocytes? Give 3 examples.

Tissue-resident macrophages that stay in one tissue for life: alveolar (lung) macrophages, Kupffer cells (liver), dendritic cells (skin).

24
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List the five classic signs of inflammation.

Rubor (redness), calor (heat), tumor (swelling), dolor (pain), and loss of function.

25
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List the stages of inflammation.

Injury/immediate reactions → vascular reactions (dilate–constrict–dilate) → edema and pus formation → resolution/scar formation.

26
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Define diapedesis.

The migration of white blood cells out of blood vessels into tissues.

27
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Define chemotaxis

Migration of cells toward a specific chemical stimulus gradient (e.g., toward a site of infection).

28
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Differentiate exudate and edema.

Exudate is fluid that escapes from blood vessels; edema is the local swelling caused by accumulation of that fluid in tissue.

29
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What is pus composed of?

White blood cells (mainly neutrophils) plus liquefied cellular debris and bacteria.

30
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What does 'pyogenic' mean? Give examples.

Pus-producing; e.g., streptococci, staphylococci, gonococci, and meningococci are pyogenic bacteria.

31
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What is a fever and what controls body temperature?

An abnormally elevated body temperature; set-point is maintained by the hypothalamus (normally ~37°C/98.6°F).

32
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Differentiate exogenous and endogenous pyrogens.

Exogenous pyrogens come from outside the body (microbial products, toxins, vaccines); endogenous pyrogens are released by host cells (e.g., IL-1, TNF from monocytes/macrophages/neutrophils).

33
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List three benefits of fever.

Inhibits multiplication of temperature-sensitive microbes; reduces bacterial access to iron; increases metabolism and stimulates immune reactions (e.g., speeds phagocytosis).

34
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What are interferons and their three main types?

Small antiviral/immune-regulatory proteins; IFN-alpha and beta (from lymphocytes, fibroblasts, macrophages) and IFN-gamma (from T cells).

35
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How does interferon protect neighboring cells?

t's secreted and binds receptors on nearby host cells, inducing proteins that degrade viral RNA and block viral protein synthesis; it is not microbe-specific.

36
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What is complement?

A system of over 30 blood proteins that work in a cascade to destroy bacteria, certain viruses, parasites, and other cells.

37
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List the 4 stages of the complement cascade.

1) Initiation: C3 → C3a + C3b.

2) Activation/cascade: C3b cleaves C5 → C5a + C5b.

3) Polymerization: C5b + C6-C8 form the membrane attack complex (MAC).

4) Membrane attack: MAC forms pores → cell lysis.

38
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Differentiate the classical and alternative complement pathways.

Classical requires antibody already bound to the microbe to initiate; alternative doesn't require antibody, is triggered by foreign antigens directly, and is faster.

39
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What are antimicrobial peptides? Give an example family.

Short proteins (12–50 amino acids), e.g., defensins, that insert into bacterial membranes and form pores, causing lysis.

40
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What are the four major categories of the second line of defense?

Phagocytosis, inflammation, fever, and antimicrobial products (interferon, complement, antimicrobial peptides).

41
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What does lysozyme do and where is it found?

An enzyme in tears and saliva that hydrolyzes peptidoglycan in bacterial cell walls.

42
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How does the normal microbiome contribute to the first line of defense?

It forms a structural barrier blocking pathogen access to epithelial surfaces, competes for nutrients, and alters local pH.

43
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Name the four body systems that participate in the first line of defense.

Integumentary (skin), digestive, respiratory, and genitourinary systems (mucous membranes throughout).

44
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What makes the third line of defense different from the other two?

It is acquired individually after exposure to a specific antigen (infection or vaccination), is highly specific, and has memory — unlike the general, nonspecific first two lines.

45
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 Differentiate antigen, immunogen, and epitope

Antigen = any molecule the immune system can recognize; immunogen = an antigen that actually provokes an immune response; epitope = the specific site on an antigen recognized by an antibody/receptor.

46
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Define immunocompetence.

The ability of the body to react against countless different foreign substances

47
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List the four stages of an adaptive immune response.

1) Lymphocyte development & clonal deletion.

2) Antigen presentation & clonal selection.

3) Challenge of B and T lymphocytes by antigen.

4) T-cell response (cell-mediated) and B-cell response (antibody production).

48
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What is the MHC?

The major histocompatibility complex — a set of genes coding for human cell surface markers (also called the HLA system); central to self-recognition and antigen presentation

49
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Differentiate MHC Class I, II, and III genes.

Class I: markers on all nucleated cells (self ID). Class II: on macrophages, dendritic cells, B cells; present antigen to T cells. Class III: encode complement proteins.

50
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What are CD molecules?

'Cluster of differentiation' — a naming system for cell-surface markers; CD3, CD4, and CD8 are the most important in immunity.

51
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What do CD4 and CD8 do?

CD4 is a coreceptor on T helper cells that binds MHC class II; CD8 is a coreceptor on cytotoxic T cells that binds MHC class I.

52
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Where do B and T cells mature, and where do they migrate afterward?

B cells mature in bone marrow, T cells mature in the thymus; both then migrate to and recirculate through lymph nodes, spleen, and other lymphoid tissue.

53
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How do B-cell and T-cell antigen receptors differ?

B cells bind free/unprocessed antigen directly; T cells only bind antigen that has been processed and is complexed with MHC on a presenting cell.

54
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List the three functional types of T cells.

Helper T cells, regulatory T cells, and cytotoxic T cells.

55
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What do helper T cells do?

Activate macrophages, assist B-cell processes, and help activate cytotoxic T cells — they secrete cytokines but do NOT produce antibodies.

56
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What do cytotoxic T cells do?

Destroy infected host cells, cancer cells, and foreign (grafted) cells via direct lysis; require MHC class I recognition.

57
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What happens when B cells are activated by antigen?

They divide and differentiate into plasma cells (secrete antibodies) and memory cells.

58
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Compare B cells and T cells: site of maturation, surface marker, and MHC requirement.

B cells: bone marrow, immunoglobulin receptor, no MHC required, produce antibodies. T cells: thymus, T-cell receptor + CD markers, MHC required, cell-mediated functions.

59
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What is clonal selection?

The mechanism by which the one pre-programmed B or T cell whose receptor exactly fits an incoming antigen is activated.

60
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What is clonal deletion?

The process by which self-reactive lymphocyte clones are destroyed during development, producing immune tolerance.

61
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What is clonal expansion?

Mitotic proliferation of an activated lymphocyte clone into a larger population, all sharing the same antigen specificity.

62
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How is immunologic diversity generated?

By extensive rearrangement of gene segments coding for antigen receptors during B- and T-cell development (an estimated 10 trillion possible antibody specificities).

63
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Describe the basic structure of an immunoglobulin (antibody).

A Y-shaped molecule with two heavy and two light chains; the two Fab arms bind antigen (variable regions), the Fc stem is constant and mediates effector functions.

64
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How do T-cell receptors differ from B-cell receptors (immunoglobulins)?

TCRs are relatively small, are never secreted, and bind antigen only when complexed with MHC; B-cell receptors can be secreted as free antibody.

65
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What features make a 'good' immunogen?

Foreignness, larger size, and chemical complexity (proteins are usually more immunogenic than repetitive polysaccharides); context/cytokines present also matter.

66
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What is a hapten?

A small foreign molecule too small alone to trigger an immune response; becomes immunogenic when bound to a larger carrier molecule, serving as the epitope.

67
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What are alloantigens?

Cell-surface markers/molecules that differ among members of the same species — the basis of blood groups and MHC incompatibility in transfusions/transplants.

68
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What are superantigens?

Bacterial toxins that are potent, nonspecific stimulators of T cells (activating them ~100x normal), causing overwhelming cytokine release; linked to toxic shock syndrome.

69
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Name the main antigen-presenting cells (APCs).

Macrophages, B cells, and dendritic cells.

70
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What are T-cell-independent antigens?

Antigens (e.g., repetitive polysaccharides like LPS or pneumococcal capsule) that can activate B cells directly, without APCs or T helper cells.

71
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Compare TH1, TH2, TH17, and Treg cells.

TH1: drives cell-mediated immunity/activates macrophages. TH2: helps B cells/antibody response, involved in allergy. TH17: promotes inflammation. Treg: suppresses/controls immune response, prevents autoimmunity.

72
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What do perforins and granzymes do?

Released by cytotoxic T cells: perforins punch pores in the target cell membrane; granzymes are enzymes that enter through the pores and trigger apoptosis.

73
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Differentiate NK cells and NKT cells.

NK cells are innate lymphocytes that kill abnormal cells nonspecifically; NKT cells are hybrid cells with both T-cell receptors and NK-like killing activity.

74
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What are innate lymphoid cells (ILCs)?

Innate immune cells (ILC1, ILC2, ILC3, and NK cells) that mirror T helper/cytotoxic T cell functions but lack antigen receptors and do not undergo clonal expansion

75
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List the five main antibody functions.

Opsonization, neutralization, agglutination, lysis (via complement), and antitoxin activity.

76
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List the five immunoglobulin classes and one key fact for each.

IgG: most abundant, crosses placenta. IgA: mucosal secretions, dimer form. IgM: first antibody made, pentamer, B-cell receptor early on. IgD: B-cell receptor. IgE: mediates allergy and anti-parasite response.

77
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Which immunoglobulin crosses the placenta?

IgG.

78
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Which immunoglobulin is produced first in a primary immune response?

IgM.

79
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Compare the primary and secondary immune responses.

Primary: first exposure, slower onset, lower titer (IgM then IgG). Secondary: faster and stronger due to memory cells, mostly IgG, occurs on re-exposure.

80
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Differentiate natural and artificial immunity.

Natural immunity is acquired through normal biological experiences (infection, mother-to-infant transfer); artificial immunity is acquired via medical procedures (vaccines, immune serum).

81
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Differentiate active and passive immunity.

Active: body produces its own antibodies/memory, slow onset, long-lasting. Passive: receives preformed antibodies, no memory, immediate but short-term protection.

82
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Give an example of natural passive immunity.

Antibodies passed from mother to fetus/infant via the placenta or breast milk (colostrum).

83
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What are gamma globulins?

Immunoglobulins extracted and concentrated from the pooled blood of many human donors, used for passive immunization.

84
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Who developed the first vaccine, and how?

Edward Jenner (1796); he used material from cowpox lesions to protect a boy against smallpox

85
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List the qualities of an ideal vaccine.

Protects against the natural pathogen, low toxicity/side effects, stimulates both antibody (B-cell) and cell-mediated (T-cell) responses, produces long-term memory, needs few doses, and is inexpensive, stable, and easy to give.

86
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List the major types of vaccine preparations.

Live attenuated, killed/inactivated, subunit, conjugate, mRNA, and viral vector vaccines.

87
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Give an example each of an mRNA vaccine and a viral vector vaccine.

mRNA: Pfizer and Moderna COVID-19 vaccines. Viral vector: Johnson & Johnson COVID-19 vaccine.

88
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What are adjuvants?

Substances added to vaccines that enhance immunogenicity, prolong antigen retention at the injection site, and help engage the innate immune system.

89
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What is herd immunity?

A phenomenon where a sufficient percentage of a population is immune, making it difficult for a pathogen to circulate and protecting the unvaccinated.

90
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What is a booster shot? Give two examples of schedules.

A repeat vaccine dose to maintain long-term protection; e.g., tetanus every 10 years, measles booster at age 5–6.

91
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Describe the three phases of vaccine clinical trials.

Phase 1: 20–100 volunteers, tests safety. Phase 2: several hundred volunteers, tests short-term side effects/immune response. Phase 3: hundreds to thousands, compares vaccinated vs. unvaccinated for safety and effectiveness.

92
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What is VAERS?

The Vaccine Adverse Event Reporting System — collects and analyzes reports of adverse events following vaccination, submitted by anyone including patients and providers.

93
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What are the three major categories of microbial identification techniques?

Phenotypic, immunologic, and genotypic.

94
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Define phenotypic identification.

Identification based on observing a microbe's macroscopic/microscopic morphology, physiology, and biochemical properties.

95
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Define immunologic (serologic) identification.

Identification using antibodies — either known antibodies to identify an unknown microbe, or known antigens to detect a patient's antibodies.

96
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Define genotypic identification.

Identification based on analysis of a microbe's DNA or RNA.

97
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Why is rapid identification critical in bloodstream infections (sepsis)?

Sepsis is a medical emergency; standard culture-based identification takes too long, increasing mortality risk, so broad-spectrum antibiotics are started immediately and narrowed once the organism is known.

98
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Why is aseptic technique important in specimen collection?

It prevents contamination of the sample from the environment or the patient's own normal microbiota, which could lead to misidentification.

99
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Differentiate 'clean catch' and 'dirty catch' urine samples.

Clean catch: midstream urine collected after washing the external urethra, minimizing normal flora contamination. Dirty catch: first-voided urine, needed for certain diagnostic tests.

100
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Which stains are used for immediate direct examination of specimens?

Gram stain (bacteria), acid-fast stain (Mycobacterium), and KOH stain (fungi).