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RNC Infectious Diseases Complete Questions and Answers latest Updated 2025

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Host defense mechanisms - -Overall functions of the immune system. a. Defense—resistance to infection by microorganisms. b. Homeostasis—removal of worn-out cells. c. Surveillance—perception and destruction of mutant cells. 2. Components of the immune system. a. The nonspecific mechanisms, which include phagocytosis, the inflammatory response, and several amplification systems including complement, coagulation, and kinin systems. b. The specific immune responses, which consist of cell-mediated (T cell) and humoral (B cell) systems. (1) Both are interdependent and interrelated; for example, the activation of the complement system by immunoglobulins (IgM and IgG), or the production of chemotactic factors and other lymphokines, plays a significant role in the whole inflammatory response. (2) Nonspecific immune mechanisms—function without prior exposure, identified early in gestation, functional development at 32 to 33 weeks. c. Embryologic development (Table 32-1). (1) The maturation of specific immune responses begins in utero during the 7th to the 12th weeks of gestation. (2) Progenitor cells (stem cells) are initially located in the yolk sac, fetal liver, and bone marrow of the developing embryo. d. Depending on the type of microchemical environment surrounding the tissue, the stem cells will differentiate along at least two pathways: (1) The hematopoietic. (2) The lymphopoietic. (a) The lymphopoietic system develops along two independent pathways leading to morphologically and functionally distinct populations of immune systems: (i) The thymus-derived or T system of cell-mediated immunity whose principal effector cells are the T lymphocytes. (ii) The bursal-dependent or B system of humoral or antibody-mediated immunity, which is displayed by the B lymphocytes. (3) The thymus gland is derived from epithelium of Humoral Immunity - -1. Immunoglobulin (McCance and Huether, 2002; Polin et al., 2001). a. Humoral immunity is a specific antibody-mediated response that functions most effectively if there has been previous exposure. b. Antibodies are derived from B cells, which have been activated by T cells and antigens (Fig. 32-1). (1) B cells mature and are stored in lymph tissue and bone marrow. (2) B cells also produce memory cells that recognize antigens on subsequent exposures and initiate an antibody response. (3) Antibody functions include: (a) Recognition of bacterial antigens. (b) Neutralization or opsonization of foreign substances, rendering them susceptible to phagocytosis. 2. Types of immunoglobulin. a. Immunoglobulin G (IgG). (1) Major immunoglobulin of serum and interstitial fluid. (2) Provides immunity against bacterial and viral pathogens. (3) Placental transfer to the fetus is either an active or a passive process. (4) Increases gradually until 40 weeks of gestation (majority is passed in the third trimester). (5) Decreased levels in preterm infants, proportional to their gestational age. (6) Decreased levels in postmature and small for gestational-age infants, suggesting inhibition of transfer with placental damage. b. Immunoglobulin M (IgM). (1) Does not cross the placental barrier. (2) Synthesis begins early in fetal life, with detectable levels at approximately 30 weeks of gestation. (3) Levels may increase (20 mg/ml) with intrauterine infection. (4) Serum levels rapidly increase after birth. c. Immunoglobulin A (IgA). (1) Is the most common immunoglobulin in the gastrointestinal and respiratory tracts and is secreted in human colostrum and human milk. (2) Does not cross the placental barrier. (3) Intrauterine synthesis is minimal in an uninfected fetus. (4) Does not beco Cellular Immunity - -1. Specific cellular immunity is mediated by T lymphocytes, which enhance the efficiency of the phagocytic responses. a. T lymphocytes migrate to the thymus, where they begin differentiation (see Fig. 32-1). b. They are activated by antigens to which they have become sensitized and subsequently become memory or activated T cells. However, they must be "processed" and presented on the surface of antigen-presenting cells (i.e., macrophages and monocytes). (1) Memory cells respond at a later time to the same antigen. (2) There are three types of activated T cells. (a) Cytotoxic: kill foreign or virus-infected cells. (b) Helper: enable B or T cells to respond to antigens and activate macrophages. (c) Suppressor: repress responses of specific T and B lymphocytes to antigens. (3) T lymphocytes modify the behavior of phagocytic cells, produce a variety of cytokines, and increase their antimicrobial activity. (4) Depressed T-cell function may occur as a consequence of neonatal viral infection, hyperbilirubinemia, corticosteroid therapy, or maternal medications taken late in pregnancy. 2. Nonspecific cellular immunity is an inflammatory response involving phagocytosis and includes neutrophils, monocytes, and complement. Neutrophilic cell invasion and platelet aggregation are aided by the activation of the three important plasma protein systems (the complement, clotting, and kinin systems) and immunoglobulins. Additionally, some host cells produce soluble factors that contribute to defenses by affecting other neighboring cells. These factors are known as cytokines and include interleukins, interferons, and other proteins. Cytokines are multifunctional proteins, often referred to as "hormones of the immune system." a. Neutrophils are phagocytes and must detect them and move toward them (chemotaxis), adhere to Summary of neonatal immunodeficiencies - -Humoral immunity. a. Decreased antibody levels. (1) Poor response to antigenic stimuli. (2) No production of type-specific antibodies. (3) Fewer B cells recognize foreign antibodies. (4) Delay in the development of cytotoxic T lymphocytes, increasing the risk for viral infections. b. Decreased opsonic activity. (1) Impaired circulating antibody. (2) Maternal complement is not transferred. (3) Depressed complement (classical and alternate) pathways and decreased levels of components of the complement cascade (50% to 80%) of adult values and less in the premature infant. 2. Neutrophil response. a. Diminished size of neutrophil storage and proliferative pools. b. Reduced numbers of immature neutrophils in the storage pool. c. Failure to increase stem cell proliferation during infection. d. Abnormal neutrophil function (adhesion, chemotaxis, phagocytosis, and bacterial killing). Vertical Transmission of infectious organism: Mother to fetus - -1. Transplacental acquisition. a. Transplacental hematogenous transmission (crosses from the placenta to the fetus). (1) Treponema pallidum and Listeria monocytogenes. 2. Ascending acquisition: into the uterus near time of delivery, when the cervical mucous plug, chorion, and amnion are less than optimal barriers. 3. Intrapartum acquisition: natal transmission at delivery, during passage of the fetus through a birth canal that is host to a variety of bacteria, as well as chlamydiae, fungi, yeast, and viruses. This mechanism implies colonization of the skin, mucous membranes, gastrointestinal tract, and respiratory tract during parturition. Horizontal Transmission of infectious organism - -from nursery personnel and the hospital equipment to the infant; also known as a nosocomial infection. Predisposing factors: Antepartum - -a. Inadequate prenatal care. b. Inadequate nutrition. c. Low socioeconomic status. d. Recurrent abortion. e. Substance abuse. f. History of maternal sexually transmitted diseases. Predisposing factors: Intrapartum - -a. Prolonged rupture of membranes (12 to 18 hours). b. Vaginal group B streptococcal colonization. c. Low levels of maternal group B streptococcus (GBS) antibodies. d. Chorioamnionitis: sustained fetal tachycardia, uterine tenderness, purulent amniotic fluid, foul-smelling amniotic fluid, or unexplained maternal temperature higher than 38°C. e. Prolonged or difficult labor. f. Premature labor. g. Urinary tract infection. h. Invasive intrapartum procedures. i. Maternal fever. j. Elevated maternal heart rate (100 beats per minute [bpm]). k. Elevated fetal heart rate (160 bpm). Predisposing factors: neonatal - -1. Prematurity (infants born 32 weeks of gestation have a 4 to 25 times increased risk). 2. Low birth weight (2500 g). 3. Difficult delivery. 4. Birth asphyxia. 5. Meconium staining. 6. Resuscitation. 7. Congenital anomalies (i.e., abdominal wall a

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RNC Infectious Diseases Complete
Questions and Answers latest Updated
2025

Host defense mechanisms - -Overall functions of the immune system.
a. Defense—resistance to infection by microorganisms.

b. Homeostasis—removal of worn-out cells.

c. Surveillance—perception and destruction of mutant cells.

2. Components of the immune system. a. The nonspecific mechanisms, which include
phagocytosis, the inflammatory response, and several amplification systems including
complement, coagulation, and kinin systems.

b. The specific immune responses, which consist of cell-mediated (T cell) and humoral
(B cell) systems. (1) Both are interdependent and interrelated; for example, the
activation of the complement system by immunoglobulins (IgM and IgG), or the
production of chemotactic factors and other lymphokines, plays a significant role in the
whole inflammatory response.

(2) Nonspecific immune mechanisms—function without prior exposure, identified early
in gestation, functional development at 32 to 33 weeks.

c. Embryologic development (Table 32-1). (1) The maturation of specific immune
responses begins in utero during the 7th to the 12th weeks of gestation.

(2) Progenitor cells (stem cells) are initially located in the yolk sac, fetal liver, and bone
marrow of the developing embryo.

d. Depending on the type of microchemical environment surrounding the tissue, the
stem cells will differentiate along at least two pathways: (1) The hematopoietic.

(2) The lymphopoietic. (a) The lymphopoietic system develops along two independent
pathways leading to morphologically and functionally distinct populations of immune
systems: (i) The thymus-derived or T system of cell-mediated immunity whose principal
effector cells are the T lymphocytes.

(ii) The bursal-dependent or B system of humoral or antibody-mediated immunity,
which is displayed by the B lymphocytes.


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,RNC


(3) The thymus gland is derived from epithelium of

Humoral Immunity - -1. Immunoglobulin (McCance and Huether, 2002; Polin et al.,
2001).
a. Humoral immunity is a specific antibody-mediated response that functions most
effectively if there has been previous exposure.

b. Antibodies are derived from B cells, which have been activated by T cells and
antigens (Fig. 32-1).
(1) B cells mature and are stored in lymph tissue and bone marrow.
(2) B cells also produce memory cells that recognize antigens on subsequent
exposures and initiate an antibody response.
(3) Antibody functions include: (a) Recognition of bacterial antigens.

(b) Neutralization or opsonization of foreign substances, rendering them susceptible to
phagocytosis.

2. Types of immunoglobulin. a. Immunoglobulin G (IgG). (1) Major immunoglobulin of
serum and interstitial fluid.

(2) Provides immunity against bacterial and viral pathogens.

(3) Placental transfer to the fetus is either an active or a passive process.

(4) Increases gradually until 40 weeks of gestation (majority is passed in the third
trimester).

(5) Decreased levels in preterm infants, proportional to their gestational age.

(6) Decreased levels in postmature and small for gestational-age infants, suggesting
inhibition of transfer with placental damage.



b. Immunoglobulin M (IgM). (1) Does not cross the placental barrier.

(2) Synthesis begins early in fetal life, with detectable levels at approximately 30 weeks
of gestation.

(3) Levels may increase (>20 mg/ml) with intrauterine infection.

(4) Serum levels rapidly increase after birth.

c. Immunoglobulin A (IgA). (1) Is the most common immunoglobulin in the
gastrointestinal and respiratory tracts and is secreted in human colostrum and human
milk.

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, RNC



(2) Does not cross the placental barrier.

(3) Intrauterine synthesis is minimal in an uninfected fetus.

(4) Does not beco

Cellular Immunity - -1. Specific cellular immunity is mediated by T lymphocytes, which
enhance the efficiency of the phagocytic responses. a. T lymphocytes migrate to the
thymus, where they begin differentiation (see Fig. 32-1).
b. They are activated by antigens to which they have become sensitized and
subsequently become memory or activated T cells. However, they must be "processed"
and presented on the surface of antigen-presenting cells (i.e., macrophages and
monocytes). (1) Memory cells respond at a later time to the same antigen.

(2) There are three types of activated T cells. (a) Cytotoxic: kill foreign or virus-infected
cells.

(b) Helper: enable B or T cells to respond to antigens and activate macrophages.

(c) Suppressor: repress responses of specific T and B lymphocytes to antigens.

(3) T lymphocytes modify the behavior of phagocytic cells, produce a variety of
cytokines, and increase their antimicrobial activity.

(4) Depressed T-cell function may occur as a consequence of neonatal viral infection,
hyperbilirubinemia, corticosteroid therapy, or maternal medications taken late in
pregnancy.

2. Nonspecific cellular immunity is an inflammatory response involving phagocytosis
and includes neutrophils, monocytes, and complement. Neutrophilic cell invasion and
platelet aggregation are aided by the activation of the three important plasma protein
systems (the complement, clotting, and kinin systems) and immunoglobulins.
Additionally, some host cells produce soluble factors that contribute to defenses by
affecting other neighboring cells. These factors are known as cytokines and include
interleukins, interferons, and other proteins. Cytokines are multifunctional proteins, often
referred to as "hormones of the immune system." a. Neutrophils are phagocytes and
must detect them and move toward them (chemotaxis), adhere to

Summary of neonatal immunodeficiencies - -Humoral immunity.
a. Decreased antibody levels.
(1) Poor response to antigenic stimuli.
(2) No production of type-specific antibodies.
(3) Fewer B cells recognize foreign antibodies.
(4) Delay in the development of cytotoxic T lymphocytes, increasing the risk for viral
infections.

RNC

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