Fire Ant Stings and Other Mishaps:
Immnology
Donna Sullivan, PhD
Host Defensive Systems
 1st line of defense  intact skin
 mucous membranes and their secretions
 2nd line of defense  phagocytic white blood cells
 inflammation
-complement
 fever
-interferon
 3rd line of defense B and T lymphocytes
 antibodies
2
nonspecific
specific
Physical or anatomical barriers
 Outermost layer of skin is composed of epithelial cells






3
compacted, cemented together and impregnated with
keratin
Flushing effect of sweat glands
Damaged cells are rapidly replaced
Mucous coat impedes attachment and entry of bacteria
Blinking and tear production
Stomach acid
Nasal hair traps larger particles
Chemical Defenses
 Sebaceous secretions
 Lysozyme, an enzyme that hydrolyzes






4
the cell wall of bacteria, in tears
High lactic acid and electrolyte
concentration in sweat
Skin’s acidic pH
Hydrochloric acid in stomach
Digestive juices and bile of intestines
Semen contains antimicrobial
chemical
Vagina has acidic pH
DIFFERENTIATION OF CELLS
5
Leucocytes
 Granulated: granules, lobed nuclei
 Neutrophils
 Eosinophils
 Basophils
 Agranulated: un-lobed, round nuclei
 Monocytes
 Macrophages, dendritic cells
 Lymphocytes
 T cells, B cells
6
GRANULOCYTES
 Neutrophils (PMNs)
 Strongly phagocytic, important in controlling bacterial
infections
 Usually first cells to arrive at site
 Eosinophils
 Weakly phagocytic, main role in allergic reactions, destruction
of parasites
 Basophils
 Non phagocytic
 Cell surface receptors for IgE
 Mediated allergic and antiparasitic responses due to release of
histamine
7
DIFFERENCES BETWEEN NEUTROPHILS
AND MACROPHAGES
NEUTROPHILS
MACROPHAGES
 Rapid increase in production
 Only slight increase in blood




8
(and in blood) during acute
phase of infection
Only found in inflamed tissues
Single mature form
Rapidly form pus
Short-lived; die after
phagocytosis
during inflammation
 Found in healthy tissues
 Multiple mature forms
 Slowly form granulomas (with T
cell help)
 Long-lived-survive after
phagocytosis
MONOCYTES/MACROPHAGES
 Released from bone marrow
 Circulate in blood and enter tissues where they mature into
macrophage
 Activated macrophage
 Initiated by phagocytosis of particulate antigens
9
CELLS OF THE MONOCYTEMACROPHAGE SYSTEM
BLOOD - MONOCYTES
LYMPH NODES RESIDENT &
RECIRCULATING
MACROPHAGES
BRAIN - MICROGLIAL
LUNGS - ALVEOLAR
SPLEEN - MACROPHAGES
KIDNEY - MESANGIAL
LIVER - KUPFFER
CONNECTIVE TISSUE HISTOCYTES
BONE MARROW
- PRECURSORS
10
JOINTS - SYNOVIAL A
MACROPHAGES: FUNCTION
 Stand guard
 Initiate early innate immune response
 Educate the specific immune system
 Present antigen associated with Class II MHC to CD4 TH cells
 Call in the troops
 Secrete cytokines that promote immune responses
 Join the battle
 Phagocytose and inactivate microbes
 Secrete antibacterial substances, inflammatory mediators, and
complement components
11
Phagocytosis
12
NATURAL KILLER CELLS
 Primary targets of NK cell killing are virus infected and
tumor cells
 May depend on reduced expression of Class I MHC molecules,
alterations in surface carbohydrates
 Mechanism of killing
 Direct cytotoxicity
 Antibody dependent cellular cytotoxicity (ADCC)
13
Stages Of Inflammation
 Blood vessels dilate in response to chemical mediators and




14
cytokines
Edema swells tissues, helping prevent spread of infection
WBC’s, microbes, debris and fluid collect to form pus
Pyrogens may induce fever
Macrophages and neutrophils engage phagocytosis
Developmental Stages of Monocytes
and Macrophages
15
INFLAMMATION
 Tissue damage due to trauma, caustic agents, microbes
 Mediated primarily by immune system cells, cytokines
 Acute inflammation
 Chronic inflammation
16
Rubor, Calor, Tumor, Dolor
 Rubor: Redness caused by increase circulation and
vasodilation in injured tissues
 Calor: Warmth, heat given off by increased flow of blood
 Tumor: Swelling, caused by increased fluid escaping into the
tissues
 Dolor: Pain, causes by stimulation of nerve endings
17
TRAUMA AND INFLAMMATION
18
TRAUMA AND INFLAMMATION
19
TRAUMA AND INFLAMMATION
20
TRAUMA AND INFLAMMATION
21
TRAUMA AND INFLAMMATION
22
Activities Of Phagocytes
 Stand guard
 To survey tissue compartments and discover microbes,
particulate matter and dead or injured cells
 Join the Battle
 To infest and eliminate these materials
 Educate Specific Immune System
 To extract immunogenic information from foreign matter
23
Chemical Mediators
24
Complement
 Consists of 26 blood proteins that work in concert to destroy
bacteria and viruses
 Complement proteins are activated by cleavage
 Classical pathway
 Alternative pathway
25
Complement
26
Specific immunities
 B and T lymphocytes
 Specificity and memory
27
28
Lymphocyte Development and
Differentiation
29
Antigen
Presentation
Challenge of B
and T Cells
B Cell Antibody
Production
T Cell
Responses
Preliminary concepts
 Cell receptors or markers confer specificity and identity
 Major functions of receptors are
 To perceive and attach to nonself or foreign molecules
 To promote the recognition of self molecules
 To receive and transmit chemical messages among other cells of
the system
 To aid in cellular development.
31
How Are Receptors Formed?
 As a cell matures, certain genes that encode cell
receptors are transcribed and translated into protein
products with a distinctive shape, specificity and
function.
 Receptor is modified and packaged by the endoplasmic
reticulum and Golgi complex.
 It is ultimately inserted into the cell membrane,
accessible to antigens, other cells, and chemical
mediators.
32
Receptor Formation in a Developing
Cell
33
Major Histocompatibility Complex (MHC)
 Receptors found on all cells except RBCs
 Also known as human leukocyte antigen (HLA)
 Plays a role in recognition of self by the immune system
and in rejection of foreign tissue
 Genes for MHC are located on chromosome 6, clustered
in a multigene complex of classes I, II, III
34
MHC Receptors
35
Functions of MHC
 Class I – markers that display unique characteristics of
self molecules and regulation of immune reactions
 Required for T lymphocytes
 Class II – receptors that recognize and react with foreign
antigens. Located primarily on macrophages and B cells
 Involved in presenting antigen to T cells
 Class III – secreted complement components, C2 and C4
36
Clonal Selection Theory
 Lymphocytes use 500 genes to produce a tremendous variety
of specific receptors
 Undifferentiated lymphocytes undergo genetic mutations and
recombinations while they proliferate in the embryo forming
a billion different clones with the ability to react with a
tremendous variety of antigens.
37
Ability to React to Every Antigen Is PreProgrammed
 Lymphocyte specificity is preprogrammed, existing in
the genetic makeup before an antigen has ever entered
the system.
 Each genetically different type of lymphocyte expresses a
single specificity.
 First introduction of each type of antigen into the
immune system selects a genetically distinct lymphocyte
and causes it to expand into a clone of cells that can react
to that antigen.
38
Structure of Antibodies
40
Immunoglobulins
 Immunoglobulin genes lie on 3 different chromosomes
 Undifferentiated lymphocyte has 150 different genes for
the variable region of light chains and 250 for the
variable region and diversity region of the heavy chain
 During development, recombination causes only the
selected V and D genes to be active in the mature cell.
41
Gene Segments of Immunoglobulins
 Heavy chains
 Variable (V)
 Diversity (D)
 Joining (J)
 Constant (C)
 Light chains
 Variable (V)
 Joining (J)
 Constant (C)
42
HYPERSENSITIVITY REACTIONS
 Type I (immediate) hypersensitivity: IgE-mediated
atopic (allergic) and anaphylactic reactions
 Type II hypersensitivity: Ab-dependent cytotoxicity
 Type III hypersensitivity: Immune complex induced
tissue damaging inflammation
 Type IV (delayed) hypersensitivity:Cell-mediated
cytotoxicity
44
45
TYPE II REACTIONS: Blood Typing and Transfusion
Reactions
46
47
TYPE IV (DTH) REACTION: TB Skin Test
48
IMMUNE REACTIONS DUE TO
MATERNAL ANTIBODIES
50
Insect Stings
 Normal reaction: local pain, erythema, swelling
 Onset 10-15 minutes
 Subsides in 1-2 hours
 Therapy: cool compresses, analgesics
Insect Stings
 Large, local reactions
 Peak at 48 hours
 Duration of 1 week
 Occasional fatigue, nausea
 Not IgE mediated
 Therapy: antihistamines, prednisone
Insect Stings
 Anaphylaxis: IgE mediated
 Generalized urticaria, flushing, angioedema, cardiorespiratory
symptoms
 Onset 15-20 minutes up to 72 hours
 Adults have highest mortality
 Prevention: avoidance, EpiPen, immunotherapy if skin test
positive
Fire Ant Stings
 Fire Ant Stings





Ferocious; potent venom; multiple stings
Intense pain followed by pruritis
Immediate flare (2-5cm) and wheal (≤1cm)
8-10 hours later a sterile pustule develops
Systemic reactions (16%) rarely life threatening
Fire Ant Stings
 Chance of being stung 50%
 Reactions
 Wheal & Flare 100%
 Pustule 96%
 Large local reaction 3.6-56%
 Secondary infection 54%
 Systemic 16%
 Cutaneous
 Life-threatening 0.6-2%
 Deaths 32
http://afrsweb.usda.gov/fireant/venom.htm?pf=1
Allergic Reaction: Possible Causes
 Insect bites/stings (bees, wasps, etc.)
 Food (nuts, crustaceans, peanuts, etc.)
 Plants
 Medications
 Others
Findings
 Skin
 Warm, tingling feeling
 Face, mouth, chest, feet, and
hands
 Itching
 Hives
Respiratory System
 Tightness in throat/chest
 Cough
 Swelling of the airway
 Rapid breathing
 Noisy breathing
 Labored breathing
 Inability to speak or cough
 Retractions
 Hoarseness
 Use of accessory muscles
 Stridor
 Wheezing (audible without
stethoscope)
RESPIRATORY FAILURE!
RESPIRATORY ARREST!
Cardiovascular System
 Increased heart rate
 Decreased blood pressure
 Decreased perfusion
(shock) due to
vasodilation
Generalized Findings
 Itchy, watery eyes
 Headache
 Sense of impending doom
 Runny nose
Other Signs and Symptoms
 Decreasing mental status
 Signs of shock (hypoperfusion)
 Respiratory distress
Emergency Medical Care
 Patient has prescribed epinephrine?
 Facilitate administration of preloaded epinephrine.
 Reassess every 2 minutes.
 No auto-injector
 CALL 911!!! Transport to ER