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Chapter 005 and 006 Pathology
- 2. Review of Body Defenses
First line of defense
Nonspecific
Mechanical barrier
Unbroken skin and mucous membranes
Secretions such as tears and gastric juices
Second line of defense
Nonspecific
Phagocytosis
Inflammation
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •2
- 3. Review of Body Defenses
(Cont.)
Third line of defense
Specific defense
Production of specific antibodies or cell-mediated
immunity
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •3
- 4. Defense Mechanisms in the Body
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •4
- 5. Normal Capillary Exchange
Generally not all capillaries in a particular
capillary bed are open.
Depend on the metabolic needs of the cells or
need of removal of wastes
Movement of fluid, electrolytes, oxygen, and
nutrients on arterial end based on net
hydrostatic pressure
Venous end—osmotic pressure will facilitate
movement of fluid, carbon dioxide, and other
wastes.
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •5
- 6. Normal Capillary Exchange Versus
Inflammatory Response
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •6
- 7. Physiology of Inflammation
A protective mechanism and important basic
concept in pathophysiology
Disorders are named using the ending –it is.
Inflammation is a normal defense mechanism
Signs and symptoms serve as warning for a
problem:
Problem may be hidden within the body.
It is not the same as infection.
Infection, however, is one cause of inflammation.
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •7
- 8. Causes of Inflammation
Direct physical damage
Examples: cut, sprain
Caustic chemicals
Examples: acid, drain cleaner
Ischemia or infarction
Allergic reactions
Extremes of heat or cold
Foreign bodies
Examples: splinter, glass
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •8
Infection
- 9. Steps of Inflammation
Injury to capillaries and tissue cells
Release of bradykinin from injured cells
Bradykinin stimulates pain receptors.
Pain causes release of histamine.
Bradykinin and histamine cause capillary
dilation.
Break in skin allows bacteria to enter tissue
Neutrophils phagocytize bacteria.
Macrophages (mature monocytes) leave the
bloodstream and phagocytose microbes.
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •9
- 10. Acute Inflammation
Process of inflammation is the same,
regardless of cause.
Timing varies with specific cause
Chemical mediators affect blood vessels and
nerves in the damaged area:
Vasodilation
Hyperemia
Increase in capillary permeability
Chemotaxis to attract cells of the immune system
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •10
- 11. Chemical Mediators in the
Inflammatory Response
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •11
- 12. Local Effects of Inflammation
Redness and warmth
Caused by increased blood flow to damaged area
Swelling (edema)
Shift of protein and fluid into the interstitial space
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •12
Pain
Increased pressure of fluid on nerves; release of
chemical mediators (e.g., bradykinins)
Loss of function
May develop if cells lack nutrients; edema may
interfere with movement.
- 14. Exudate
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •14
Serous
Watery, consists primarily of fluid, some proteins,
and white blood cells
Fibrinous
Thick, sticky, high cell and fibrin content
Purulent
Thick, yellow-green, contains more leukocytes,
cell debris, and microorganisms
- 15. Systemic Effects of Inflammation
Mild fever (pyrexia)
Common if inflammation is extensive
Release of pyrogens
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •15
Malaise
Feeling unwell
Fatigue
Headache
Anorexia
- 16. The Course of Fever
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •16
- 17. Changes in the Blood
with Inflammation
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- 18. Course of Inflammation
and Healing
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- 19. Potential Complications of
Inflammation
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •19
Infection
Microorganisms can more easily penetrate
edematous tissues.
Some microbes resist phagocytosis.
The inflammatory exudate also provides an
excellent medium for microorganisms.
Skeletal muscle spasm
May be initiated by inflammation
Protective response to pain
- 20. Chronic Inflammation
Follows acute episode of inflammation
Less swelling and exudate
Presence of more lymphocytes,
macrophages, and fibroblasts
Continued tissue destruction
More fibrous scar tissue
Granuloma may develop around foreign
object
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •20
- 21. Potential Complications
Deep ulcers may result from severe or
prolonged inflammation
Caused by cell necrosis and lack of cell
regeneration that causes erosion of the tissue
• Can lead to complications such as perforation of viscera
• Extensive scar tissue formation
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •21
- 22. Treatment of Inflammation
Acetylsalicylic acid (ASA)
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •22
Aspirin
Acetaminophen
Tylenol
Nonsteroidal anti-inflammatory drugs
(NSAIDs)
Ibuprofen
Glucocorticoids
Corticosteroids
- 23. Drugs Used to Treat Inflammation
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •23
- 24. Anti-Inflammatory Effects of
Glucocorticoids
Decreased capillary permeability
Enhanced effectiveness of epinephrine and
norepinephrine
Reduced number of leukocytes and mast
cells
Reduces immune response
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •24
- 25. Adverse Effects of
Glucocorticoids
Atrophy of lymphoid tissue; reduced
hemopoiesis
Increased risk of infection
Catabolic effects
Increased tissue breakdown; decreased protein
synthesis
Delayed healing
Delayed growth in children
Retention of sodium and water because of
aldosterone-like affect in the kidney
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •25
- 26. “RICE” Therapy for Injuries
Rest
Ice
Compression
Elevation
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •26
- 27. Types of Healing
Resolution
Minimal tissue damage
Regeneration
Damaged tissue replaced with cells that are
functional
Replacement
Functional tissue replaced by scar tissue
Loss of function
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •27
- 28. The Healing Process
Healing of incised wound by first intention
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •28
- 29. The Healing Process (Cont.)
Healing by second intention
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •29
- 30. Scar Formation
Loss of function
Result of loss of normal cells and specialized
structures
• Hair follicles
• Nerves
• Receptors
Contractures and obstructions
Scar tissue is nonelastic.
Can restrict range of movement
Adhesions
Bands of scar tissue joining two surfaces that are
normally separated
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •30
- 31. Scar Formation (Cont.)
Hypertrophic scar tissue
Overgrowth of fibrous tissue
• Leads to hard ridges of scar tissue or keloid
formation
Ulceration
Blood supply may be impaired around scar
• Results in further tissue breakdown and
ulceration at future time
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •31
- 32. Complications of Scar Tissue
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •32
- 33. Complications of Scar Tissue
(Cont.)
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •33
- 34. Burns
Thermal—caused by flames or hot fluids
Chemical
Radiation
Electricity
Light
Friction
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •34
- 35. Classification of Burns
Superficial partial-thickness (first-degree)
burns
Involve epidermis and part of dermis
Little, if any, blister formation
Deep partial-thickness (second-degree) burns
Epidermis and part of dermis
Blister formation
Full-thickness (third- and fourth-degree) burns
Destruction of all skin layers and often underlying
tissues
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •35
- 36. Classification of Burn Injury
by Depth
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •36
- 37. Examples of Burns
Partial-thickness burn
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •37
- 38. Examples of Burns (Cont.)
Deep partial-thickness burn
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •38
- 39. Examples of Burns (Cont.)
Full-thickness burn
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •39
- 40. Effects of Burn Injury
Both local and systemic
Dehydration and edema
Shock
Respiratory problems
Pain
Infection
Increased metabolic needs for healing period
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •40
- 41. Assessment of Burn Area Using
the Rule of Nines
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •41
- 43. Healing of Burns
Hypermetabolism occurs during healing
period.
Immediate covering of a clean wound is
needed to prevent infection.
Healing is a prolonged process.
Scar tissue develops, even with skin grafting.
Physiotherapy and occupational therapy may
be necessary.
Surgery may be necessary to release
restrictive scar tissue.
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •43
- 45. Microorganisms
Small living forms
Include bacteria, fungi, protozoa, viruses
Many can grow in artificial culture medium
Nonpathogenic
Usually do not cause disease unless conditions
change
Part of normal flora
Often beneficial
Pathogens
Disease-causing microbes
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •45
- 47. Bacteria
Classified as prokaryotes
No nuclear membrane—no nucleus
Function metabolically and reproduce
Divide by binary fission
Complex cell wall structure
Do not require living tissues to survive
Vary in size and shape
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •47
- 48. Reproduction by Binary Fission
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •48
- 49. Major Groups of Bacteria
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •49
Bacilli
Rod-shaped organisms
Spirochetes
Include spiral forms and Vibrio spp.
Cocci
Spherical forms
• Diplococci
• Streptococci
• Staphylococci
- 50. Basic Structure of Bacteria
Rigid cell wall
Protects and provides a specific shape
Two types that differ in chemical composition:
• Gram-positive
• Gram-negative
Useful in selecting appropriate antimicrobial
therapy
Cell membrane located inside the bacterial
cell wall
Selectively permeable
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •50
- 51. Structure of a Bacterium and Mode
of Action of Antimicrobial Drugs
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •51
- 52. Basic Structure of Bacteria
(Cont.)
External capsule or slime layer
Found in some
Outside the cell wall
Offers additional protection
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •52
Flagellae
One or more attached to cell wall
Provide motility for some species
Pili or fimbriae
Tiny hairlike structures—found in some bacteria
Assist in attachment to tissue
Transfer of DNA to another bacterium
- 53. Basic Structure of Bacteria
(Cont.)
Cell membrane
Inside the bacterial cell wall
Selectively permeable
Cytoplasm contains:
Chromosome
• One long strand of DNA
Ribosomes and RNA
Plasmids
• DNA fragments; nonchromosomal; exchange DNA
during conjugation
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •53
- 54. Basic Structure of Bacteria
(Cont.)
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •54
Toxins
Exotoxins
• Usually produced by gram-positive bacteria
Endotoxins
• Present in the cell wall of gram-negative bacteria
• Released on death of bacterium
• Vasoactive compounds that can cause septic shock
Enzymes
• Damage tissues and promote spread of infection
- 55. Spore Formation
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •55
Spores
Formed by several species
Dormant-latent form of bacterium
Can survive long periods of time in spore state
Highly resistant to heat and disinfectants
- 56. Viruses
Small obligate intercellular parasites
Protein coat or capsid
Protein coat comes in various shapes and
sizes
Can change (mutate) quickly
Nucleic acid
DNA or RNA
Classification dependent on nucleic acid present
Some RNA-containing viruses contain reverse
transcriptase enzyme to convert RNA to DNA.
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •56
- 57. Different Shapes of Viruses
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •57
- 58. Active Viral Infection
Virus attaches to host cell.
Viral genetic material enters the cell.
Viral DNA or RNA takes control of cell.
Uses host’s cell to synthesize viral proteins
and nucleic acids
New viruses are assembled in cytoplasm of
cell.
Viruses released by lysis of host cell or by
budding from host cell membrane
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •58
- 60. Latent Viral Infection
Virus enters cell as with active infection.
Viral proteins are produced and Inserted into
membrane of the host cell. This may
stimulate an immune response and
destruction of host cell.
Virus may reproduce actively if immune
system is depressed (e.g., herpesviruses)
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •60
- 61. Chlamydia, Rickettsiae,
Mycoplasmas
Obligate intercellular parasites.
Do not grow on artificial media
Some similarities with both bacteria and
viruses
Lack some basic components
Classified as bacteria
Replicate by binary fission within host cell
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •61
- 62. Chlamydia, Rickettsiae,
Mycoplasmas (Cont.)
Chlamydia
Common cause of sexually transmitted disease
Can result in infertility
Rickettsiae
Gram-negative
Transmitted by insect vectors (lice, ticks)
Mycoplasmas
Lack cell wall
Cause of atypical type pneumonia
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •62
- 63. Fungi
Eukaryotic organisms (contain nucleus)
Found throughout environment
On animals, plants, humans, food
Fungal or mycotic infection
From single-celled yeast or multicellular molds
Only a few are pathogenic.
Cause primary infection on skin or mucous
membranes but may spread systemically
particularly in immunosuppressed individual
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •63
- 65. Examples of Fungal Diseases
Histoplasma can cause neurologic disease
and can be transmitted to embryo or fetus if
mother is infected
Tinea pedis (athlete’s foot)
Candida: usually harmless, but opportunistic
Causative agent of thrush and vaginitis
Pneumocystis jirovecii
Opportunistic organism causing pneumonia
Has some characteristics of fungi and some of
protozoa
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •65
- 66. Protozoa
Eukaryotic forms
Unicellular, lack cell wall
Many live independently, others are obligate
parasites
Pathogens are usually parasites.
Examples of protozoal diseases:
Trichomoniasis
Malaria
Amebic dysentery
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •66
- 67. Other Agents of Disease
Helminths (flatworms or roundworms)
Are not microorganisms
Parasites
May be small or up to 1 m in length
Life cycle with at least three stages
• Ovum, larva, adult
Enter body through skin or by ingestion,
depending on species
Infections more commonly found in young children
Infection can be life-threatening in an
immunosuppressed client.
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •67
- 68. Helminth Diseases
Pinworms: ova inhaled in dust in fecally contaminated
areas; common in children worldwide
Hookworms: larvae enter skin from fecally
contaminated soil in tropical areas
Tapeworms: most common form transmitted by
larvae in undercooked pork
Ascaris—giant roundworm: ingested with food that
has been grown in feces-contaminated soil or
prepared with hands that have been in feces-contaminated
soil
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •68
- 69. Other Agents of Disease (Cont.)
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •69
Prions
Protein-like agents that change the shape of
proteins within host cells
Transmitted by contaminated tissues
• Ingestion of meat
• Infected blood or donor organs
Cause degenerative disease of the nervous
system
Human prion diseases
• Creutzfeldt-Jacob disease and variant Creutzfeldt-Jacob
disease
• Both rapidly progressive and fatal
- 70. Resident Flora
Many areas of the body have a resident
population of mixed microorganisms termed
normal flora.
Skin
Nasal cavity
Mouth
Gut
Vagina
Urethra
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •70
- 71. Principles of Infection
Infection—organism is able to reproduce in or
on body’s tissues
Sporadic
In a single individual
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •71
Endemic
Continuous transmission within a population
Epidemic
Higher than normal transmission or spread to new
geographical area
Pandemic
Transmission has occurred on most continents.
- 72. Transmission of Infectious
Agents
Transmission from person to person
Reservoir
Source of infection
Person with active infection
Person who is asymptomatic
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •72
Carrier
A person may never develop the disease but still
is a carrier.
A person with subclinical signs of the disease
- 73. Transmission of Infectious Agents:
Links in the Infection Chain
Agent: the microbe causing the infection
Reservoir:
Environmental source such as contaminated soil
Infected person or animal
• Person may carry the agent and show no signs of
disease
• Person or animal may show signs and symptoms of
disease
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •73
- 74. Transmission of Infectious Agents:
Links in the Infection Chain (Cont.)
Portal of exit: means whereby the agent
leaves the reservoir
Mode of transmission: method whereby the
agent reaches a new susceptible host
Air
Water
Direct contact
Food
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •74
- 75. Transmission of Infectious Agents:
Links in the Infection Chain (Cont.)
Portal of entry: access to new host
Susceptible host: susceptibility will depend
on:
Health status
Immunity
Age
Nutrition
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •75
- 77. Modes of Transmission
Direct contact
No intermediary
Touching infectious lesion, sexual activity
Contact with infected blood or bodily secretions
Indirect contact
Involves intermediary object or organism
Contaminated hand or food
Fomite—inanimate object
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •77
- 78. Modes of Transmission (Cont.)
Droplet transmission
Respiratory or salivary secretions are expelled
from infected individual
Aerosol transmission
Involve small particles from the respiratory tract
Suspended in air and can travel farther than
droplets
Vector-borne
Insect or animal is an intermediate host
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •78
- 79. Nosocomial Infections
Occur in health care facilities
Hospitals, nursing homes, physician’s offices,
dental offices
10% to 15% of patients acquire an infection in
the hospital because of:
Many microbes present
Patients with undiagnosed infectious disease
Shared environment
Treatment that may cause weakened immune
system
Many health care workers and fomites act as
reservoirs.
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •79
- 80. Host Resistance and Microbial
Virulence
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- 81. Factors That Decrease Host
Resistance
Age (infants and older adults)
Pregnancy
Genetic susceptibility
Immunodeficiency
Malnutrition
Chronic disease
Severe physical or emotional stress
Inflammation or trauma
Impaired inflammatory responses
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •81
- 82. Virulence and Pathogenicity
Pathogenicity
Capability of a microbe to cause disease
Virulence
Degree of pathogenicity
• Invasive qualities (e.g., motility or enzymes)
• Toxins
• Adherence to tissue by pili, fimbriae, specific receptor
sites
• Ability to avoid host defenses
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •82
- 83. New Issues Affecting Infection
and Transmission
Newly emerging diseases
Antigenetically different forms of common
infections such as influenza
Spread beyond normal endemic areas
Superinfections
Multidrug-resistant forms of existing diseases
• TB
• Staphylococcus aureus
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •83
- 84. Control of Transmission and
Infection
Infection control requires two approaches:
Standard Precautions used in all settings with all
clients when body fluids may be exchanged.
Specific Precautions in clients diagnosed with a
particular infection—these are used in addition to
standard precautions.
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •84
- 85. Infection Cycle and Breaking
the Chain
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •85
- 86. Break the Cycle: Provide an
Example of Each of the Actions
Locate and remove or isolate the reservoir of
infection.
Identify and restrict access to contaminated
food or water.
Reduce contact between infected persons
and the remainder of the population.
Block portals of exit and entry.
Remove or block modes of transmission.
Reduce host susceptibility by immunizations,
adequate nutrition, and access to health care.
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •86
- 87. Additional Techniques to Reduce
Transmission
Adequate cleaning of surroundings and
clothing
Sterilization
Disinfectants
Antiseptics
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •87
- 88. Physiology of Infection
Incubation period
Time between entry of organism into the body and
appearance of clinical signs of disease
Vary considerable with different organisms
Prodromal period
Fatigue, loss of appetite, headache
Nonspecific—“coming down with something”
More evident in some infections than others
Acute period
Infectious disease develops fully
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •88
- 89. Means of Disinfection
Sterilization of equipment by:
Chemicals
Heat in an autoclave
NOTE: Equipment must be cleaned prior to
sterilization or it will remain contaminated!
Use of chemicals:
Antiseptics are used on the skin and tissues.
Disinfectants are used on surfaces or objects.
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •89
- 90. Patterns of Infection
Local infections
Focal infections
Systemic infections
Septicemia
Bacteremia
Toxemia
Viremia
Mixed infections
Primary infections
Secondary infections, subclinical infections
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •90
- 92. Signs and Symptoms of Infection
Local signs of inflammation
Pain, swelling, redness, warmth
• If bacterial—purulent exudate
• If viral—serous, clear exudate
Systemic signs of inflammation
Fever may be present.
Fatigue and weakness
Headache
Nausea
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •92
- 93. Methods of Diagnosis
Culture and staining techniques
Using specific clinical specimens
Drug sensitivity tests
Blood tests
Variations in numbers of leukocytes
• Leukocytosis—bacterial infection
• Leukopenia—viral infection
Differential count
C-reactive protein
Erythrocyte sedimentation rate (ESR)
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •93
- 94. Diagnostic Tests (Cont.)
Immunological testing of body fluids
Antigen identification
Antibody titer
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •94
- 95. Guidelines for Drug Therapy
Drugs should be administered and taken as directed.
Antimicrobial drugs should be taken until prescribed
medication is completely used or until new drug is
prescribed.
If symptoms continue without reduction, contact the
pharmacist or physician.
Do not use drugs prescribed for other clients or other
infections.
If drug resistance is known to occur with infection,
use multidrug therapy.
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •95
- 96. Classification of Antimicrobials
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Antibiotic
Drugs derived from organisms
Antimicrobial
Antibacterial
Antiviral
Antifungal
Bactericidal
Drugs destroy organism
Bacteriostatic
Decrease rate of reproduction
- 97. Classification of Antimicrobials
(Cont.)
Broad spectrum
Effective against both gram-positive and gram-negative
organisms
Narrow spectrum
Effective against either gram-positive or gram-negative
organisms
First- and second-generation drugs
First generation—original drug class
Second generation—later version, which may be
more effective, more tolerable, or more easily
administered
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •97
- 98. Mode of Action of Antibiotics
Interfere with bacterial cell wall synthesis
Example: penicillin
Increase permeability of bacterial cell
membrane
Example: polymyxin
Interfere with protein synthesis
Example: tetracycline
Interfere with synthesis of essential
metabolites
Example: sulfonamides
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •98
- 99. Mode of Action of Antivirals
Drugs may act by:
Blocking entry into host cell
Inhibiting gene expression
Inhibiting assembly of the virus
•Copyright © 2014, 2011, 2006 by Saunders, an imprint of Elsevier, Inc. •99
- 100. Antifungal Agents
May interfere with mitosis in fungi
May increase fungal membrane permeability
Most antifungal agents administered topically
to skin or mucous membranes
Fungi are eukaryotic cells and are therefore
often toxic to animal and human cells.
Treatment requires strict medical supervision.
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- 101. Antiprotozoal agents
Similar characteristics to antifungal agents
Protozoans are eukaryotic cells.
Many pathogenic protozoa have several
stages in their life cycles.
Require treatment with different agents at different
stages of the cycles
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