chapter 2 Flashcards
1
Q
Causes of antibiotic resistance
A
Antibiotic Overuse – creation of ‘superbugs’ – antibiotic-resistant organisms
Methicillin-resistant Staphylococcus aureus (MRSA)
Multi-drug resistant Mycobacterium tuberculosis
Vancomycin-resistant Enterococci
Multi-drug resistant Pseudomonas aeruginosa
Fluoroquinolone-resistant Clostridium difficile
Antibiotic Resistance – Other Factors
Increased travel/exposure – with globalization
TB on the rise; 2nd leading cause of death due to infectious disease worldwide Susceptible sub-populations:
Kids in daycare
Aging
Hospital populations
3 rd world poverty – stress, poor nutrition, close quarters (easy spread), lack of medical care
-use in agriculture
2
Q
Some bacteria, all viruses, and all parasites cause illness via infection.
– Bacteria: Salmonella spp., Listeria monocytogenes, Campylobacter jejuni, Vibrio parahaemolyticus, Vibrio vulnificus, and Yersinia enterocolitica.
– Viruses: Hepatitis A, norovirus, and rotavirus.
– Parasites: Trichinella spiralis, Giardia duodenalis
A
Infection
3
Q
results when a person eats food containing toxins that cause illness.
Toxins are produced by harmful microorganisms, the result of a chemical contamination, or are naturally part of a plant or seafood.
A
Intoxication: Some bacteria cause an intoxication.
Viruses and parasites do not cause foodborne intoxication.
– Bacteria: Clostridium botulinum, Staphylococcus aureus, Clostridium perfringens, and Bacillus cereus
4
Q
Signs and symptoms – know what they are
Signs and Symptoms of Infectious Diseases
A
Many and varied Can be systemic (fever) or local (pus) Depends on: – Etiologic agent – type and virulence – System affected – Health of the individual Common Systemic Signs & Symptoms Fever Chills Sweat Malaise Nausea Vomiting Change in leukocyte type and/or number Enlarged lymph nodes Possible cognitive changes in the elderly
5
Q
– pathogenesis (pyrogen affect hypothalamus), causes, over 37 C
A
− Fever
6
Q
many types and variety of causes of rash
A
FYI Common Rashes with Infections
Maculopapular eruptions: – Measles, Rubella, Fifth Disease, Roseola
Nodular lesions: – Streptococcus, Pseudomonas
Diffuse erythema: – Scarlet Fever, Toxic Shock Syndrome
Vesiculobullous eruptions: – Varicella, Herpes zoster
Petechial purpuric eruptions: – Epstein Barr Virus
7
Q
-Can be associated with many infectious diseases, not just sepsis Easily palpated – Cervical – Inguinal – Axillary Other reasons for inflamed lymph nodes: – Cancer – Rheumatoid Arthritis – Medications
A
− Lymphangitis
8
Q
local infection spreading into the lymphatic system – Lymphangitis – Moves towards local lymph node
A
red streak
9
Q
−- Secondary to an infection Usually from: – Hemolytic Streptococcus and/or Staphylococcus
Lymph nodes most often affected: – Submandibular – Cervical – Inguinal – Axillary
A
Sepsis
10
Q
Aging We become more susceptible to infectious disease as we age:
Immunosenescence – changes in the immune system as we age
Decreased circulation and poor wound healing
Decreased function of natural barriers: – Skin; pH less acidic; fewer natural secretions to help with flushing (i.e. tears
– Decreased cough/gag reflexes · decreased ability to clear secretions
– Decreased bronchiolar elasticity and mucociliary activity · increased risk of pneumonia
A
Decreased T-cells formed, but increased memory cells
– Slower to respond/require a stronger stimulus
– Increased likelihood of reactivation of dormant infections (i.e. TB, shingles)
Co-morbidities – incidence of chronic disease rises with age
Medications – can also mask symptoms/signs
Increased risk for falls/fractures – Increased risk for infections (hospitals?)
Surgical-related infections
Dentures
Exposure higher – old age homes
11
Q
why no fever with aging?
A
– Impaired thermoregulatory system – Masking effects of drugs 1 st symptoms of infection in elderly may be: – Confusion – Memory loss – Delirium
12
Q
· Organism establishes parasitic relationship with host
· Invasion + multiplication of organism = immune response
· Damage to host:
– Microorganism’s toxins, replication, or indirectly by competing for nutrient
– By our own immune system
A
Infectious Disease
13
Q
An organism that elicits a pathologic response in the host · Depends on: · Site of invasion · Number of pathogens, and virulence · How well they disseminate in host · IMMUNE STATUS OF THE HOST
A
pathogen
14
Q
pathogens that cause disease in people with apparently intact immune systems ·
A
Principal pathogens
15
Q
pathogens that don’t cause disease in people with intact immune systems, but can cause devastating disease in hospitalized or immunocompromised people ·
A
Opportunistic pathogens
16
Q
the ability of the organism to induce disease
A
Pathogenicity
17
Q
refers to the potency of the pathogen in producing sever disease and is measured in case fatality rate
A
Virulence
18
Q
An environment in which an organism can live and multiply
Animal, plant, soil, food, organic substance
Humans
Human and animal reservoirs can be symptomatic or asymptomatic
A
A reservoir
19
Q
-where the organism leaves the reservoir Corresponds to entry point on next host
A
– A portal of exit
Examples: – Respiratory droplets, blood, vaginal secretions, semen, tears – Urine, feces – Open lesions, pus
20
Q
Contact – directly or indirectly.
– Direct = physical contact
Indirect= via an inanimate intermediate object, called a fomite.
A
– Ex. Intercourse - HIV vs. touching a handrail – enteric pathogens
21
Q
disease-causing organisms float on air currents in the room. Often propelled from respiratory tract through coughing/sneezing.
A
Airborne –– Ex. TB, Chickenpox
22
Q
different then airborne because they do not remain suspended in air but fall within 3ft of course. Produced by coughing/sneezing.
A
·Droplet – Ex. Influenza ·
23
Q
occurs when infectious organisms are transmitted through a common source to many potential susceptible hosts. – Ex. Salmonella in contaminated food
A
Vehicle
24
Q
–involves insects and/or animals that act as intermediaries between 2 or more hosts
A
·Vector
– Ex. Lyme disease via Black-legged or Deer Ticks
25
Where the pathogen invades/enters: Ingestion Inhalation Bites Contact with mucous membranes Percutaneous Transplacental
– A susceptible host · This sequence is called the “chain of transmission
A portal of entry
26
factors of host susceptibility
FACTORS:
Age, sex, ethnicity Health & nutrition Hormonal balance Co-morbidities Living conditions Personal behaviours (drug use, hygiene, diet, sexual practices)
· Medications – i.e. corticosteroids, chemo · Environment – i.e. daycare, hospitals · Use of invasive equipment – i.e. catheters, i.v. lines, chest tubes · Stress · Underlying medical disorders that specifically decrease T-cell and B-cell medicated immunity – i.e. HIV, Diabetes, Malignant cancers
27
Time between entering the host, and “infection” – Hours (GI bugs) to months (Lyme dz) – Symptoms = end of incubation – ‘latency’ = dormant
Incubation
28
– Clinical symptoms – Host-parasite interaction causes injury – Mild Fatal – Communicability: ability to spread to another host
Infection
29
smallest, RNA or DNA covered with proteins – Antibiotics don’t help – Antiviral meds only moderately effective · Entirely dependent on host · Some anti-viral meds are specific – Acyclovir - ’s DNA replication
Virus
30
Very small self-replicating bacteria with no cell wall, dependant on host for nutrition ·
Mycoplasmas
| Eg. M.hominis; M.pneumoniae
31
Single celled organisms with cell wall; independent · Replicate by growing and dividing in half – they can do this in any tissue · Classified by shape (spherical-cocci, rod-shaped - bacilli, spiral-shaped - spirochetes), staining (Gram positive/negative), motility, spores, O2 /nonO
bacteria
32
types of bacteria
aerobic and anaerobic
example-normal gut flora-anaerobic
– Staphlococcus aureus is aerobic (lungs, skin)
33
Small obligate intracellular parasites – non-motile gram negative bacteria · Primarily animal pathogens that produce disease in humans · Transmitted via insect bites (tick, flea, louse, mite) · Require host for replication · i.e. Q Fever (Coxiella); “Trench Fever” carried by lice (Rochalimaea)
Rickettsiae
34
Smaller than bacteria but larger than viruses – Obligate intracellular - Dependent on host for replication – Always contain both RNA and DNA (unlike viruses) – Susceptible to antibiotics – curative - Most common STD - Leading cause of P.I.D. - Leading cause of preventable blindness in neonates
Chlamydiae
35
Unicellular organism that produce hyphae (filamentous outgrowths) · Contain nuclei (eukaryotic) · Cell walls · Yeasts or molds · Reproduce by budding off · Eg. Candida albicans
Fungi (yeast/mold)
36
-large, multicellular organisms that are generally visible to the naked eye in their adult stages. · can be either free-living or parasitic in nature. · In their adult form, helminths cannot multiply in humans. There are three main groups of helminths: – Flatworms (platyhelminths) – these include the trematodes (flukes) and cestodes (tapeworms). – Thorny-headed worms (acanthocephalins) – Roundworms (nematodes) – the adult forms of these worms can reside in the gastrointestinal tract, blood, lymphatic system or subcutaneous tissues.
Helminths (worms)
37
Single cells or groups of cells · Motile, free living in moist environments · Cell membrane, no cell wall · Divide similar to bacteria · Eg. Giardia
protozoa
38
Most common bacterial pathogens on the skin
| · Over 30 spp. – only a few relevant ones ·
Staphylococcus
39
· Transmission: – Direct contact – nasal passages most common; also skin, axilla, perineum, vagina, oropharynx · Risks: – Insulin-dependant Diabetics; HIV+; hemodialysis; IV drugs; chronic skin lesions; corticosteroid use; surgery; burns · Pathogenesis: – Secretes membrane-damaging enzymes & toxins – Stimulate a strong host immune response
S.aureus
S. aureus is the most virulent
· Leading cause of nosocomial and community acquired infections · 13% of all hospital infections = 2 million/year leading to 60,000-80,000 deaths per year · All ages · Blood,skin, lung, soft tissue, joints, bones · Gram +
40
· Clinical Manifestations of s.aureaus
– suppuration (pus) and abscess formation
– eg. Boils, pus filled vesicles – respiratory tract infection (esp. in newborns), osteomyelitis, infections of burns and surgical wounds, septicemia, Toxic Shock Syndrome, bacterial arthritis, bacterial endocarditis, impetigo – Consumption of S.aureus toxins in contaminated food is common cause of food poisoning – Fever, chills, and diffuse erythema, pain, swelling
S. aureus · Diagnosis: culture from infected site, blood, or other fluids · Must test for antibiotic resistance · Prognosis: good with tx, unless MRSA – if untreated systemic (e.g. endocarditis) – MRSA
41
· one of most common bacterial pathogens of humans · Causes many diseases: · Skin infection, pharyngitis (“Strep Throat”), rheumatic fever, » suppurative - invasion of site with necrosis and pus acute inflammation » non-suppurative - away from site of invasion, immune related and triggered by previous strep infection (Eg. rheumatic fever) · S/Sx: fever, chills, sore throat, enlarged lymph nodes, skin inflammation · Usually transmitted via respiratory droplets
· Group A Streptococcus (S. pyogenes)
42
“Strep Throat” · Most common in children, 5-10 y. old · Incubation: 1-5 days · Clinical Manifestations: · sore throat with pain on swallowing, · beefy red pharynx, · tonsillar exudates, · swollen tonsils and uvula, · swollen regional lymph nodes, · malaise and weakness, · anorexia · Can also colonize with no symptoms · Complications: otitis media, sinusitis, or rarely arthritis, endocarditis, meningitis, etc
Streptococcal Pharyngitis ·
43
Usually follows untreated Strep throat – pyogenic exotoxin is released Kids ages 2-10 Clinical Manifestations: – Sore throat, – fever, – strawberry tongue, – Rash which starts on upper chest, spares palms/soles Desquamation of palms and soles later on
Scarlet fever-strawberry tongue
44
Serious infection that progresses rapidly along fascial planes Usually in legs Causes severe tissue damage Used to be called Streptococcal gangrene Edema, tenderness, pain, fever
Necrotizing Fasciitis
45
– Most common cause of neonatal pneumonia, meningitis, sepsis – Fatal in 3-4% of neonates
– Normal vaginal flora in 30% females · may be passed on to baby as it passes through birth canal – Only 1% of these babies develop infection – Infection in baby: hypotension, pneumonia, bacteremia, meningitis – This is the reason moms are put on antibiotics just before delivery due date
Streptococcus agalactiae
| (group B strep
46
is a very important gram + organism because it is a major cause of bacterial pneumonia and meningitis in adults, and otitis media in children
Etiology & Risk Factors – post-influenza or viral URTI, chronic disease, immunosuppression, alcohol abuse
Clinical Features of Strep Pneumoniae pneumonia: – acute fever, chills – pleuritis w/ pleuritic chest pain – Dyspnea – productive cough or purulent sputum - possibly blood-streaked
streptococcus pneumococcus(group b strep)
47
·· Etiology: severe trauma, wartime injury, septic abortion · Pathogenesis: – death of tissue with loss of vasculature, bacterial invasion, fermentation gas and putrefaction (decomposition) · Clinical Features: <3 days after injury-sudden severe pain- dishcahrge with foul-odour- prognosis-possimbly amputation, extremities better better than visceral or trunk
Clostridium Perfringes – Gram + – gas gangrene
48
Gram positive bacteria Spread through aerosol or skin shedding's Range from asymptomatic carriage to life-threatening syndrome that includes pharyngitis and toxin-mediated damage to heart, nerves, and other organs.
Corynebacterium Diphtheria
49
– aerobic gram negative opportunistic pathogen, spread by contact Most common nosocomial pathogens
Uncommon in healthy populations
Thrives in pools, tubs (moist environ.)
Pneumonia, wound infections esp. burns, sepsis, UTIs, osteochondritis Inherently antibiotic-resistant
Pseudomonas
| P. aeruginosa
50
· Gram-negative coffee bean-shaped diplococci aerobic bacteria · Neisseria gonorrhoeae (gonococcus) - responsible for the sexually transmitted infection gonorrhea · Neisseria meningitides (meningococcus) – significant cause of bacterial meningitis
Neisserial Infections
51
is a Gram-negative, rodshaped coccobacillus, a facultative anaerobic bacterium that can infect humans and animals. It causes the deadly disease named plague
Yersinia pestis
52
most common · Hepatitis
· Hep B, C and HIV
53
spread through sex, blood or placenta – Vaccine available ·
hep b( viral infection
54
- spread through blood – No vaccine available ; ·
hep C -viral infection
55
– retrovirus that causes HIV infection and Acquired Immunodeficiency Syndrome – infects CD4+ T cells · Bodily fluid transfer
Human Immunodeficiency Virus
56
Mucosal contact = initial transmission After first outbreak, becomes latent in sensory ganglia Periodic lifetime outbreaks with certain triggers (a bad cold, high stress, decreased immune function, etc.)
Herpesviruses (HSV)
57
herpes simplex virus type
```
· Type 1 (HSV 1) – cold sores – 70% population ·
Type 2 (HSV 2) – Genital – 20% population – birth canal infection ·
type 3- · 1 o form: – highly contagious 1-2 days before vesicular rash · 2 o form: Herpes Zoster – 10- 20% reactivated dermatome pattern
```
58
– mucosal contact, lymph/blood spread – 95% between 35-40years of age have been infected · Fever, rash, fatigue, lymphadenopathy, spleen enlargement · Possibly involved in later development of FM, CFS, and MS
Type 4 – EBV (Epstein Barr virus)
| Infectious Mononucleosis - “the kissing disease”
59
· 80% pop’n are carriers, esp. with AIDS · transmission: all fluid except saliva, spread via lymphocytes · usually asymptomatic/self-limiting · In immunocompromised - fever, splenomegaly, hepatitis, blindness, peripheral neuropathy
Type 5 · Cytomegalovirus (CMV)
| Type 6 & 7 – B & T-cell viruses associated with roseola (or 6 th disease) – Rash – Fever – Runny nose
60
– associated with Karposi’s sarcoma in AIDS
Type 8
61
– Outbreaks common in winter & spring
– Large droplet transmission or direct contact
– Sxs: high fever, chills, malaise, myalgia, HA, sore throat, congestion, nonproductive cough
influenza(respiratory virus)
62
– Leading cause of lower resp. infections in children worldwide – Mild in older children/adults – “common cold”
Respiratory Syncitial Virus (RSV)
63
– Many strains – some cause · cervical cancer · Genital warts
Human Papilloma virus – DNA viruses
64
– almost eradicated · Rarely causes poliomyelitis
Poliovirus
65
bacteria Borelia burgdorferi – Vector - deer, bear or black-legged tick
· Stage I – 1 st 2 weeks; localized; “bull’s-eye” rash flu-like Sx ·
Stage 2 – early disseminated, rash resolved, Lyme arthritis unilateral swelling large joints, fatigue, loss of appetite
· Stage 3- (50% of untreated) intermittent arthritis, profound fatigue, chronic neuropathy, bone erosion · Tx: prevention, antibiotics
lyme disease
66
transmission: sex, sharing needles, vaginal birth ·
STI’s ·
67
– the cause of 99.9% of cervical cancer; also genital warts common in men · Chlamydia – most common
HPV – Human Papilloma Virus
68
can lead to neo-natal blindness and P.I.D. ·
Syphilis – 3 stages: · Painless chancre · Warty lesion · Very bad complications [granulomas, CVD, neuropathologies, CNS infection, insanity]
STI
69
– painful urination; pus discharge from urethra, P.I.D. in female partner, sterility/ectopic pregnancy – cured with antibiotic, but serious Antibiotic resistance now
Gonorrhea
70
– (Tinea corporis): the fungi spread, forming a ring shape with a red, raised border. This expanding raised red border represents areas of active inflammation with a healing center.
· Ringworm
71
- Superficial fungal infection which leads to hypopigmented or hyperpigmented patches on the skin.
Tinea Versicolor
72
Can infect the mouth, groin or vagina. Also an opportunistic infection. ·
Candidiasis
73
– opportunistic fungal infection causing pneumonia
Pneumocystis carnii
74
-Develops embryologically from the venous system · It’s main job: take up extra fluid · Physiological functions in the body: – Maintain fluid level – Fight infections – Remove cellular waste/debris from extracellular spaces
Lymphatic System
75
Inflammation of a lymph vessel
Lymphangitis
76
- Inflammation of one or more lymph nodes
Lymphadenitis
77
Increased lymph fluid in the tissues
Lymphedema
78
Accumulation of lymphatic fluid in tissue chronic inflammation progressive tissue fibrosis decreased tissue oxygenation and increased risk of infection (decreased activity of macrophages) · exacerbated by further infection (cellulitis or lymphangitis) or inflammation · Sequelae: – Delayed wound healing, possible necrosis
Pathogenesis of lymphedema
79
swelling, pain, paraesthesia (tingling), ROM, loss of function · Stemmer’s sign – thick skinfold over 2nd toe
Clinical Manifestations of lymphedema
80
Enlargement of the lymph nodes
Lymphadenopathy
81
· The complement cascade has multiple pathways that converge to form:
Membrane attack complex
82
Pathology is:
the study of disease
83
Natural Killer cells are a part of which immune system?
Innate
84
Which of the following describes lymphedema?
Increased lymph fluid in the tissues
85
Your patient come to you complaining that their child has a sore throat, fever, really red tongue that looks almost like a strawberry and a rash everywhere but there palms/sole. She most likely has caused by .
Scarlet fever; Group A strep (Strep pyogenes)
86
An increase in the size of the tissue caused by an increase in the number of cells, is called:
Hyperplasia
87
, white blood cells, called B lymphocytes (B cells), make antibodies
that attack pathogens in the blood.
In humoral immunity
88
In white blood cells, called T lymphocytes (cytotoxic and helper T
cells), mobilize other immune cells and find and destroy abnormal or infected cells
cell-mediated immunity
89
The response is the body’s response to specific invader
adaptive/acquired
90
A substance that triggers the immune response is known as a (n)
antigen .
91
The main role of antibodies
is to tag antigens/microbes for destruction by immunesystem cells
92
The main working cells of the immune system are two types of
lymphocytes
93
___________ can recognize these hidden organisms and destroy the cells
T-lymphocytes
94
differentiate into Memory cells or plasma cells.
b-lymphocytes
95
What type of B cell is produced that acts immediately against antigens once contact with a Thelper cell has occurred. How do these cells stop antigens from infecting other cells?
Plasma cells – create antibodies that mark them for destruction
96
8. Considering adaptive immunity, why is the secondary response to a previously identified
pathogen so much faster than the primary response?
Memory cells
97
What is a major histocompatibility complexes?
Cells fingerprint – identifies self from non-self
98
Discuss specificity as it relates to acquired immunity. How can this system be so specific in
response? Where does the basis for the specificity come from?
Each antigen has a specific B cell or T cell that will responds to it. Identifying different
epitopes of different antigens.
99
an increase in body temperature which slows or stops
| pathogens
fever
100
a secretion of the nose and throat that stops pathogens
mucus
101
c. an enzyme found in the tears and saliva that breaks down bacteria cell walls
. lysozyme
102
chemicals that increase blood flow to tissues
. histamines
103
combination of physical and chemical barriers that defend
| against pathogens
exterior defenses
104
redness, swelling and pain at the site of an injury
inflammatory response
105
proteins that fight viral growth
interferons
106
. the body’s most important nonspecific defense
skin
107
. the body’s most important nonspecific defense
skin
108
Series of interconnected events & a dynamic process
-Acute (sudden and stats for a brief period of time) vs. Chronic (stays for a long time)
Occurs only in multicellular organisms – must be able to mount a neurovascular and cellular response
Protective and usually beneficial
Occurs only in living tissue
Inflammation
109
Nonspecific, predictable response of tissue or entire body to injury. Causes:
Chemical agents
Physical force
Microbes
Any other stimuli that disturbs normal steady state
110
Signs of Inflammation
Four cardinal signs of inflammation (Celsus 30 BC-38 AD) must know!
Heat (calor)
Redness (rubor)
Swelling (tumor)
Pain (dolor)
Loss of function (function laesa - added later in 1900)
111
Five classical signs of inflammation
```
(Acronym – SHARP or PRISH)
Swelling
Heat
Altered Function/Immobility
Redness
Pain
```
112
Inflammatory Process
Inflammation is a complex process that includes:
1. Changes in circulation of blood
2. Changes in vessel wall permeability
3. White blood cell response
4. Release of soluble mediators
113
A. Vasoconstriction of arterioles – last only seconds
B. Vasodilation (muscle release histamine)
A mechanical stimulus stimulates nerves to relax the smooth muscle cells on precapillary arterioles → blood rushes into capillaries → redness, swelling, warm tissue
Hyperemia (increase redness)
C. Edema – fluid leaks out of blood vessels
D. Pain
Direct trauma
Pressure from edema
Chemical mediators
Swelling of nerve endings
1. Circulatory Changes – first response to injury
114
Changes in permeability of capillary and post capillary venule walls occurs because of:
A. Increased pressure inside congested blood vessels
B. Slowing of circulation → reduces oxygen and nutrient supply
C. Adhesion of platelets → Release of soluble mediators of inflammation
D. Adhesions of leukocytes (white blood cells) to endothelial cells – pavementing
2. Vessel Wall Changes
| D. Adhesions of leukocytes (white blood cells) to endothelial cells – pavementing
115
- the act or process of forming a margin specifically : the adhesion of white blood cells to the walls of damaged blood vessels.
1 Margination
116
-A condition occurring during inflammation in which leukocytes adhere to the linings of capillaries.
2 Pavementing
Attach to endothelium = pavementing
Protrusions from cytoplasm stick to endothelial cells (especially postcapillary venules)
117
movement of a motile cell or organism, or part of one, in a direction corresponding to a gradient of increasing or decreasing concentration of a particular substance.
4 Chemotaxis
118
-a mass of cells and fluid that has seeped out of blood vessels or an organ, especially in inflammation.
5 Exudate
119
is extravascular fluid with low protein content and a low specific gravity (< 1.012). It has low nucleated cell counts (less than 500 to 1000 /microliter) and the primary cell types are mononuclear cells: macrophages, lymphocytes and mesothelial cells.
6 Transudate-
120
invasion of site with necrosis and pus acute inflammation
7 Suppurative-
121
(from Ancient Greek φαγεῖν (phagein) , meaning 'to eat', and κύτος, (kytos) , meaning 'cell') is the process by which a cell uses its plasma membrane to engulf a large particle (≥ 0.5 μm), giving rise to an internal compartment called the phagosome. It is one type of endocytosis.
8 Phagocytosis-
122
is the process of forming grains or granules from a powdery or solid substance, producing a granular material. It is applied in several technological processes in the chemical and pharmaceutical industries.
9 Granulation tissue
123
a type of raised scar. They occur where the skin has healed after an injury. They can grow to be much larger than the original injury that caused the scar. Anything that can cause a scar can cause a keloid. This includes being burned, cut, or having severe acne
10 Keloid-
124
is when a surgical incision reopens either internally or externally. Although this complication can occur after any surgery, it tends to happen most often within two weeks of surgery and following abdominal or cardiothoracic procedures.
11 Wound Dehiscence-
125
- is the capability of multicellular organisms to resist harmful microorganisms from entering it. Immunity involves both specific and nonspecific components. The nonspecific components act as barriers or eliminators of a wide range of pathogens irrespective of their antigenic make-up
12 Immunity
126
the branch of medicine and biology concerned with immunity.
13 Immunology-
127
having a normal immune response.
14 immunocompetence-
128
-a toxin or other foreign substance which induces an immune response in the body, especially the production of antibodies.
15 antigen
129
-a blood protein produced in response to and counteracting a specific antigen. Antibodies combine chemically with substances which the body recognizes as alien, such as bacteria, viruses, and foreign substances in the blood.
16 antibodies
130
, group of genes that code for proteins found on the surfaces of cells that help the immune system recognize foreign substances. MHC proteins are found in all higher vertebrates. In human beings the complex is also called the human leukocyte antigen (HLA) system.
17 MHC-Major histocompatibility complex (MHC)
131
the part of an antigen molecule to which an antibody attaches itself.
18 Epitope -
132
-refers to the gradual deterioration of the immune system brought on by natural age advancement. The adaptive immune system is affected more than the innate immune system.
19 Immunosenescence
133
· Organism establishes parasitic relationship with host · Invasion + multiplication of organism = immune response
20 Infection-
134
Microorganisms can be present, but not cause symptoms · “colonization of organisms” · You could be carrier – can transmit to other people and be ‘infectious’ while also non-symptomatic
21 Carrier-
135
pathogens that cause disease in people with apparently intact immune systems
22 Principal Pathogen-
136
-pathogens that don’t cause disease in people with intact immune systems, but can cause devastating disease in hospitalized or immunocompromised people
23 Opportunistic Pathogen
137
– refers to the potency of the pathogen in producing sever disease and is measured in case fatality rate
24 Virulence e
138
– the ability of the organism to induce disease
25 Pathogenicity -
139
Also know which are examples of diseases that HAIs Nosocomial infections – Originating or taking place in a hospital, acquired in a hospital, especially in reference to an infection. – A.k.a. Hospital acquired infections (HAI) – Most common are UTIs (from catheters or urologic procedures), blood infections (from IV catheters or surgical wounds), and GI infections
26 Nosocomial (HAIs)
140
– occurs when infectious organisms are transmitted through a common source to many potential susceptible hosts. – Ex. Salmonella in contaminated food
27 Vehicle
141
(leukocyte rolling across endothelium)
Move through the blood vessel wall to inflamed tissue
Phagocytosis → swelling and pain
D. Emmegration (aka transmigration)
Emigration leads to exudate
Exudate – fluid containing more protein than transudate and also polymophonuclear leukocytes or polymophonuclear neutrophils (PMNs) (the first WBC to reach the problem area)
Within first 48 hours of inflammation
Exudate contains a high concentration of PMNs, monocytes, eosinophils
Lifespan of only 2-4 days
142
Chemical mediators – Histamine,
```
Histamine
Released by mast cells and platelets
Causes contraction of endothelial cells of venules → gaps → increased blood vessel
permeability
Vasodilator and bronchoconstrictor
Lasts less than 30 minutes
```
143
Bradykinin,
Plasma protein formed by Hageman factor (Coagulation factor XII)
Same effects as histamine but at a slower pace
Causes pain
144
– several proteins that are activated in a cascade acting on one another Numbered 1-9 (C1, C5..)
All pathways converge to form the Membrane Attack Complex (MAC) (key to destruction of foreign agent)
Bores holes into membranes of microbes or body’s owncells
Fill with fluid → cell death
Complement System
3 pathways that activate the complement cascade
1. Classical pathway – activated by antigen-antibody complexes.
2. Alternative pathway – activated by bacterial endotoxins, fungi, snake venom
3. Lectin pathway – activated by binding of lectin to bacteria
145
Derived from phospholipids of cell membranes
Form leukotrienes and prostaglandins
Polyunsaturated fatty-acid found in brain, muscle and liver
Arachidonic Acid Derivatives
146
increase vascular permeability and promote chemotaxis
Formed through the LOX pathway (lipoxygenase pathway)
Bronchospasm – contract smooth muscles in bronchi
Anaphylactic shock
Leukotrienes –
147
- Stimulate vasodilation, increase vascular permeability
Formed through the COX pathway (cyclooxygenase pathway)
Pain and fever
Prostaglandins
148
WHITE BLOOD CELLS (AKA. LEUKOCYTES)
Neutrophils (Most abundant)
Eosinophils
Basophils → Mast Cells
Monocytes → Macrophages (macrophages form monocyte) (macrophages found in tissues)
Lymphocytes → Plasma Cells (not all lymphocytes will form plasma cells)
Cells of Inflammation
149
2-3% of circulating WBCs
Appear 2-3 days After PMNs in area of inflammation
Longer lifespan – chronic inflammation
Like PMNs they are mobile, phagocytic and bactericidal
nteract with basophils
Allergic reactions – hay fever, asthma
Respond to parasitic infection (Mainly hellmas parasite, round worm, hook work and tape worm)
Eosinophils
150
Less than 1% of circulating WBCs
Most prominent in allergic reactions (IgE)
Cytoplasmic granules contain histamine
Precursors to Mast Cells
Basically basophils outside of the blood vessel
Basophils
151
```
Derived from monocytes in blood
Large
Appear at site of inflammation 3-4 days after onset of infection or injury
Long-lived
Chronic inflammation
Phagocytosis and release cytokines
```
Macrophages MUST KNOW
152
**two main phagocytic cells =
Monocytes/Macrophages and Neutrophils”
153
Released from megakaryocytes in bone marrow
No nucleus
Cytoplasm contains vacuoles and granules
Histamine, coagulation proteins, cytokines, growth factors
Release histamine in early stages of inflammation
Platelets (not cells, they are cellular fragments)
154
Classification of Inflammation
Acute
Sudden onset
Hours to days
Eg. Common cold, ankle sprain
```
Chronic
Weeks to months to years
May be result of:
Recurrent acute inflammation
Prolonged healing of acute inflammation
Persistence of causes of inflammation
Due to prolonged duration it produces more extensive tissue destruction, heals less
readily, and is associated with more functional deficiencies.
```
155
Etiology – what caused the inflammation
```
Infectious
Bacterial, viral, protozoal, fungal, helminthic
Chemical – organic or inorganic
Physical
Heat, trauma, foreign body
Immune – to be discussed shortly
Location
Localized or Systemic
Boil – local vs Sepsis (= bacteremia or septicemia) - systemic
```
156
Produce extracellular matrix
Fibronectin – provides the glue to hold cells together in wound healing
Fibroblasts
| Collagen – from fibrils in interstitial spaces
157
Properties of smooth muscle cells and fibroblasts
Contract like muscle cells and secrete cell matrix substances like fibroblasts
Holds edges of damaged tissue together
myofibroblasts
158
Precursors of blood vessels
Proliferate from small blood vessels at the edges of damaged tissue
Appear 2-3 days after injury. By day 6 new blood vessels are formed
Provide a route for scavenger cells to remove tissue debris and scabs
Allow oxygen and nutrients to flow to injured site
Angioblasts (angio = vessels)
159
Vascularized tissue filled with macrophages, myofibroblasts, angioblasts, fibroblasts
Turns into a scar
Granulation tissue
160
```
Site of wound
Mechanical factors
Size of wound
Presence or absence of infection
Circulation issues
Nutritional and metabolic factors
Age
```
Wound Healing
Depends on:
161
Deficient scar formation – poor formation of granulation tissue
Inadequate collagen production can lead to wound dehiscence
Complications of Wound Healing
Excess scar formation
Keloid scar – hypertrophic scars
Can lead to disfigurement and loss of function
162
Immune Response
Innate Immunity (born with)
Nonspecific, protective
No memory
Acquired Immunity
Specific
Has memory
163
1st line of defence
Physical Barriers – Exterior Defenses
Skin – best defense we have
Shown when significant burns occur –infection is a major problem
Mucosa – body openings have their own
defences
Tears – lysozymes protect the eyes, wash away
foreign substances
Ears – ciliated, ear wax
Stomach and duodenal - low pH values (acidic)
Vagina – acidic
Urine – acidic
164
Innate Immunity
2nd line of defence – cells and inflammation
Phagocytes
1. Neutrophils
2. Monocytes
3. Macrophages
```
Cells that release inflammatory mediators
1.Basophils
2.Eosinophils
3.Mast cells
4,Complement system
```
Natural Killer Cells
Interferons
165
Large granular lymphocytes that are neither T or B lymphocytes
Function is to kill viruses, infected cells, and tumor cells
Bind to potential target cells – release cytotoxic granules, and cytokines
Natural killer cells burst forth from the tonsils, lymph nodes and spleen, and destroy infected and cancerous cells while the immune system's T and B cells are still mobilizing
Without natural killer cells, threatening conditions can get a strong foothold before the adaptive immune response kicks in
Natural Killer cells
166
Act as messengers, within the immune system and between the immune system and
other systems of the body
- are produced by virally infected cells early in infection to limit the spread of infection by protecting surrounding (noninfected) cells
-once a cell is infected by a virus, certain genes are turned on in the cell that will produce these interferons that coat the surrounding cells to make them viral resistant
Inhibit tumor growth
Interferons
167
Acquired Immunity
Based on specific responses elicited by Antigens
Antigen – any chemical substance that can induce a specific immune response
Specific
Antigen specific – remembers the Antigens to an immune response can be mounted faster and more effectively
Has memory
Our bodies create immunologic memory to distinguishes self from non-self
Immunocompetence – ability to mount an appropriate immune reaction
168
Immunity acquired by introduction of an antigen into the host
environmental exposure
Vaccination
Active Immunity
169
Immunity acquired when antibodies produced by one person are transferred to another
trans placental transfer, breast milk, antibody inoculation
Passive Immunity
| Does not form memory cells; therefore, is only temporary immunity (lasting a few weeks to months)
170
Very small cells, round nucleus, very little cytoplasm
Derived from bone marrow stem cells and turn into one of two different lineages
Bone marrow stem cells → migrate to the thymus →T lymphocytes
Bone marrow stem cells → remain and mature in bone marrow → colonize lymphoid tissues as B lymphocytes
Lymphocytes
Primary lymphoid organs – bone marrow and thymus
T and B lymphocytes enter blood circulation and colonize secondary lymphoid organs
Lymph nodes
spleen
Also form mucoca-associated lymphoid tissue (MALT)
Gastrointestinal mucosa
Bronchial mucosa
171
Mature in thymus
Part of Cell-Mediated Immunity
2/3rds of all lymphocytes in the blood, lymph nodes and spleen
All express protein CD3 on their membrane
Linked to T-cell receptor
Used to recognize antigens
```
T Lymphocytes
Several sub-types of T lymphocytes
T Helper cells
T Suppressor cells
Cytotoxic cells
```
172
Express protein CD4 (aka CD4 cells)
75% of all T-cells
Assist B-cells to mature and produce antibody secreting protein mediators called lymphokines (ie. IL-1 and interferons)
Activate macrophages – help to destroy bacteria
Help other T-cells recognize and destroy virally infected cells (CD8 = cytotoxic T-cells)
Help NK cells kill infected cells
HIV destroys or inactivates helper T-cells, leaving the body at risk for infections
T helper cells (“master regulator”)
173
Suppress activation of the immune system and prevent pathologic self-reactivity (auto-immune disease)
T suppressor cells
174
Express CD8 antigen on their surface
| Mediate the killing of virus infected cells or tumor cells
Cytotoxic T cells
175
Differentiate into immunoglobulin producing plasma cells or memory B Cells
Part of Humoral Immunity
B Lymphocytes
Memory B-cells
circulate among the blood, lymphoid system, and tissues for 1 year or longer
-responsible for more rapid and sustained immune response that occurs with repeated exposure to the same antigen
Plasma cells
Fully differentiated B lymphocytes
Produce immunoglobulins (antibodies) (Ig)
Surface of plasma cell is coated with Ig
5 types of antibodies produced
176
Major anti-bacterial and anti-viral antibody
most abundant type in blood
Only antibody to cross placenta
Responsible for the protection of the newborn for the first 6 months of life
IgG
177
primary or initial immune response
Largest antibody
stays in blood vessels
IgM
178
```
Defends external body surface
Found on mucous membranes
Found in secretions
Saliva
Breast milk
Urine
Seminal fluid
Tears
Nasal fluid
```
IgA
179
Controls lymphocyte activation or suppression
| Found exclusively on B-cells
IgD
180
Primary factor in eliminating parasitic infections
Functions during allergic reactions
Activates mast cells to release histamine
Associated with anaphylaxis, hives, allergen induced asthma
IgE
181
Two Types of Acquired Immunity
)
182
Mediated by Antibodies (Ab) present in body fluids or secretions
Humoral = body fluids
Blood, Lymph, Interstitial Fluid
Aka. Antibody-Mediated Immunity
B Lymphocytes
Formed in bone marrow
Mature in bone marrow
Differentiate into Memory B-cells or plasma cells
Plasma cells secrete Immunoglobulins (Antibodies) to mount an immune response
Bind Antigen to display it for destruction
Memory B-cells
‘remember’ Antigen after first exposure
Acquired Immunity - Humoral
1. Humoral - B Lymphocytes (B-cells)
Protects against extracellular microbes and their toxins (eg. bacteria
183
All viruses and some bacteria hide inside cells where antibodies cannot reach them
T-lymphocytes can recognize these hidden organisms and destroy the cells
Also implicated in transplant rejection, hypersensitivity reactions, and some autoimmune diseases
```
Interaction with antigen→ activates T-lymphocyte to produce specialized Tcells (or sensitized T-cells):
Helper T-cells (75% of all T-cells)
Cytotoxic T-cells
Suppressor T-cells
Memory cells
```
2. Cell Mediated – T Lymphocytes (T-cells)
Defense against intracellular microbes (eg. viruses)
184
Lines of Defense
1st line of defense- skin, mucosal, hair, pH barriers
INNATE
2nd line of defense – inflammation
INNATE
3rd line of defense - immune system cells
ACQUIRED
