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infectivity
the ability of a pathogen to establish an infection in a host.
e.g. a highly infectious virus (like the common cold) spreads easily but may not cause severe illnesss
virulence
the relative capacity of a pathogen to cause damage or severe disease
e.g. a highly virulent pathogen (like ebola) causes severe, often fatal, illness but may be less easily transmitted
toxigenecity
the ability of the pathogen to produce harmful toxins that increase host cell and tissue damage
antigenicity
the level to which a pathogen is viewed by the host immune system as foreign
a more antigenic pathogen elicits a more prominent immune response
a less antigenic pathogen can readily elude immune mechanisms and continue to survive in the host
antigenic variability
a process of eluding the human host defenses and is often a result of altering the antigens present within or on the surface of the microorganism
(infectious organisms escaping defenses, responsible for much of the infectious disease burden in the world)
pathogenic defense mechanisms
the ways in which many pathogens have developed ways to avoid destruction by the host
e.g. thick protective capsules to prevent phagocytosis
confection
a phenomenon of hosting two or more pathogens simultaneously; presents a greater challenge to the immune system
superinfection
when an infection arises in addition to one that is already present; often results from compromised host defenses and over proliferation of resident flora (microorganisms that live within one’s body)
________ require the host for metabolism and reproduction
obligate parasites
_______ may live on the host but can also survive independently (e.g. Helminths)
facultative parasites
single-celled
most can reproduce outside of host cells
those that require oxygen for growth are aerobic
those that do not are anaerobic
bacteria
_________ _________ require oxygen for survival and for multiplication sufficient to cause disease
aerobic bacteria
anaerobic bacteria
bacteria that do not require oxygen to survive
thrive in deep tissues of the body where oxygen supply is limited
Why are anaerobic bacteria infections difficult to treat?
antimicrobial drugs often travel within the vascular system to affect local tissues
the cytoplasm of bacteria
cytosol
independent survival
bacteria can survive outside the human host and can infect and reinfect if not destroyed
structural properties critical to pathogenicity of bacteria
independent survival,
stimulation of inflammatory response
bacterial capsule
endotoxin
endospores
Bacteria stimulate this response, resulting in destruction of the surrounding host tissue in an effort to rid the body of the invader
inflammatory response
bacterial capsule
composed of chemicals not recognized as foreign
slippery and difficult for phagocytes to engulf
a toxic component of the outer membrane of certain gram-negative bacteria that is released only when the bacteria die
complex of phospholipid-polysaccharide molecules that form the structural component of the gram-negative cell wall.
causes inflammatory mediators to be released
leading to a massive inflammatory response
→ septic shock, severe diarrhea, fever, and leukocytosis
endotoxin
endospores
a thick-walled protective spore that forms inside a bacterial cell and resists harsh conditions
survive in a latent state that is resistant to environmental extremes and lack of nutrients
emerge when the environment is more conducive to replication
exotoxins
many bacteria are capable of producing these, which results in host cell dysfunction or lysis
potent bacterial-derived proteins released into surrounding tissues that cause local or systemic injury to the host → brain, GI tract, liver or blood
viruses
obligate intracellular parasites (cannot replicate outside of the host cell)
bind to specific receptors on the host cell and move into the host cell, converting the host cellular metabolism to nucleic acids and proteins that are encoded and controlled by it
can directly kill cells or modify certain cellular functions
can cause cells to proliferate rapidly and randomly, causing tumors to form in the body
virions
particles released by viruses outside of the cell which can enter and infect other nearby cells
Determined by
(1) the size of the virus that is inoculated into the body;
(2) the process of viral replication;
(3) the viral genotype;
(4) host susceptibility
chronic viral infections
latency
characteristic of chronic viral infections
a period of dormancy during which the virus is integrating itself into the host cell’s genetic material
minimal or no loss of functional capabilities of the host cell
low antigencity
active viral replication can be triggered weeks to years after the initial inoculation
e.g. herpes simplex virus, herpes zoster virus
rickettsiae
obligate intracellular parasites
gram negative bacteria capable of producing energy
target human epithelial cells of the blood vessels and capillaries
mycoplasmas
lack cells walls and survive on the surface of host cells
do not enter host cell for replication
chlamydiae
reproduce through binary fission yet are obligate intracellular parasites
use the host metabolism to reproduce
cause epithelial cell necrosis
fungi
relatively large organisms compared to bacteria and viruses
have a nuclear membrane, cytoplasm, and organelles
unicellular forms are yeasts
multicellular forms are molds
yeasts
produce by budding and form an elongated chain called pseudohypahe
mold
colonies have tubules that branch to form hyphae;
clusters of hyphae are called mycelium, mycoses
mycoses
infections with fungi
cause disease when the host’s defenses are compromised or when they grow in part of the body that is not natural to them
fungal infections can be these
opportunistic pathogens
protozoa
unicellular, complex microorganisms characterized by an irregular or fluctuant shape without a cell wall
many are motile
some are parasites and capable of living independent of the host
infectious agents
Bacteria
Fungi
Viruses
Rickettsiae
Protozoa (sterilization)
reservoirs
people, equipment, water
how do you break the chain of infection at the reservoir stage?
sanitizing environment, antimicrobial drugs
portal of exit
excretions, secretions, skin, droplets
What are some direct methods used to block or control the portal of exit, preventing infectious agents from escaping a host and spreading to others?
Hand washing, covering secretions, trash disposal
Means of transmission
Direct contact, ingestion, formats, airborne
What are some ways to interrupt means of transmission and stop the spread of disease?
(hand washing, sterilization, universal precautions, airflow control, food handling, isolation)
Portal of entry
Mucous membrane, GI tract, GU tract, respiratory tract, broken skin
What are some ways to interrupt the portal of entry
Cover
susceptible hosts
Immunosuppression, diabetes, surgery, burns, old age
What are some ways to protect a susceptible host?
Reconition of high-risk patients, treatment of underlying diseases
vector transmission
transmission of an infectious agent by an insect, arthropod, or animal (a vehicle harbors the pathogen and carries it to the host)
prodrome
subclinical illness
disease present but few symptoms
low-grade fever, nausea, weakness, and generalized muscle aches
described a feeling under the weather
incubation
this phase extends from exposure to the onset of any signs or symptoms
the individual has no idea that he or she has been exposed
during this period, transmission of microorganisms to others is greatest (for chicken pox this period is 7-21 days from exposure to recognize symptoms)
convalescence
this phase extends from waning clinical manifestations to full recovery from the disease
fatigue is common during this period
septic shock
a process of systemic vasodilation due to severe infection, often with gram-negative bacteria (the endotoxin component)
influenza
a viral infection of the epithelial cells of the airway; transmitted via respiratory droplets
impairs cilia, mucus, and antibodies then moves into the cells and replicates
well adapted to escape host defenses
gradually changes genetic composition during replication in the human host cell in a process called reassortment
viral offspring w/ altered antigenic properties result in ongoing host susceptibility to the virus
tests have a false-positive or false-negative error rate of 20-30%
hepatitis
damage to the hepatocytes inhibits bile production and can affect fat emulsification and absorption
blood glucose fluctuations
Kupffer cells
aged red blood cells are engulfed and destroyed by these phagocytes houses in the liver
small capillaries perfuse the liver and are lined with these
they readily engulf harmful substances
because of these, bacteria pose less harm to the liver than viruses
separate hemoglobin into heme and globin
erthropoeisis
the formation of red blood cells
viral hepatitis
acute or chronic liver disease
generally caused by fecal-oral contamination leads to acute, blood and body fluid exposure lead to chronic
chronic is represented by impaired liver function for more than 6 months
the liver is infiltrated with macrophages and lymphocytes
risk of developing hepatocellular carcinoma related to persistent cell injury
Clinical manifestations of viral hepatitis
prodrome (fatigue, anorexia, malaise, HA, low-grade fever; lasts about 2 weeks)
Icterus (onset of jaundice, dark urine, clay-colored stools 2 weeks after exposure to virus; lasts approximately 2-6 weeks)
Recovery (resolution of jaundice around 8 weeks after initial exposure; signs/symptoms improve, but liver remains enlarged for an addition 1-4 weeks)
diagnostic criteria for viral hepatitis
Detection of viral antibodies (anti-HAV, anti-HCV, anti-HDV, anti-HEV)
HbsAg may be present in acute infection or in those who are chronic asymptomatic carriers
bilirubin in the urine
elevated serum bilirubin (>30 mg/dL means severe disease)
prolonged clotting time
tuberculosis
caused by an aerobic, rod-shaped bacterium
primary site of infection is the lungs, but can affect any organ in the body
upon encountering bacilli, alveolar macrophages ingest but are unable to destroy the bacteria
bacilli proliferate within the macrophages, and they present the bacilli as antigens to the T lymphocytes (cell-mediated immunity)
bacilli do not produce toxins; damage to the lung and other body tissues is through hypersensitivity reaction elicited by the bacilli
formation of a granuloma as a result of the inflammatory response (goon focus) with a center called a caseous necrosis that is pasty, yellow, and cheese-like
ghon complex
the Ghon focus and additional granulomas that develop through the lymph channels
scar tissue and calcification results in these
small numbers of dormant bacteria can survive within the calcifications for years
cavitations
area of necrosis that erode surrounding structures of the lungs, including
bronchioles, bronchi, and surrounding blood vessels
secondary TB is marked by these in an aggressive and destructive form
UTI
Based on a urine culture noting greater than 1,000 colonies of a single organism per mL
bacterial meningitis
Inflammation of the membranes of the brain and spinal cord
most common bacterial cause: aerobic, gram negative bacterium
13 different types
mode of transmission: respiratory droplets that enter the respiratory tract and attach to epithelial cells
inflammatory and immune response is waged
immunoglobulins in the respiratory mucosa can provide protective immunity
viral meningitis
often referred to as aseptic meningitis
generally less severe than other types
often resolves without specific treatment
fungi can result in meningitis in immunocompromised individuals
Kernig sign
extension of the upper leg places a stretch on the meninges and causes pain
patient is placed supine with knees bent and hips flexed and moves leg upward
diagnostic criteria for meningitis
Brudzinski sign
A positive sign of meningitis, where there is an involuntary flexion of the arm, hip, knee when the patients neck is passively flexed
diagnostic criteria for meningitis
What is the treatment for bacterial meningitis
Antibiotics (IV ASAP)
Isolation (24–48 hr droplet precautions)
Rehydration (careful fluids)
Breathing support
Reduce ICP (dexamethasone, mannitol)
Alleviate stimulation
Intervene for complications
Nurture/support the family
AIRBRAIN
Tinea
group of fungal skin diseases that occur in various locations
tine pedis (feet)
tinea unguium (nails)
tine capitis (scalp); use wood light to diagnose
tine cruris (groin)
tine corpori’s (ringworm) and versicolor (skin)
tx is topical or oral anti-fungal agents (2-8 weeks)
topical therapy ineffective for tx of hair and nails (dermatophyte-ski, hair, and nails)
dermatophyte attaches to and produced thickening of keratinized cells
malaria
Caused by infection with plasmodium protozoa transmitted by mosquitos
plasmodium falciparum is the most lethal species responsible for 95% of deaths in sub-Saharan Africa
plasmodia enter circulating RBCs and feed on hemoglobin and other proteins within the cells
Infection typically develops within a month of exposure
headache, shivering and chills, high fever, excessive sweating, cough fatigue, malaise and joint/muscle aching
high fatality due to cerebral malaria
fungal meningitis
type of meningitis that commonly occurs in immunocompromised
mild sx