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virulence
ratio of the number of people exposed to microorganisms versus the number of cases of disease
doesn’t take a lot of exposure to have high numbers behind that sickness
infectivity
proportion of exposures needed to cause infection in an individual, based on the pathogens ability to enter, survive, or multiply in
toxigenicity
ability to produce harmful toxins
antigenicity
how much is it viewed as foreign by the host immune system
antigenic variability
eluding the host
coinfection
simultaneous occurence of two or more pathogens
superinfections
over proliferation of resident flora (secondary infection)
overuse or incomplete use of antibiotics leads to:
drug-resistance microbes
leukopenia
decrease in white blood cell count
leukocytosis
increase in white blood cell count
malaise
feeling ill
hemoptysis
blood sputum with chronic cough
anorexia
appetite loss
cystitis
inflammation of the bladder
pyelonephritis
infection moves from the liver (cystitis) to the kidneys
dysuria
pain with urination
hematuria
blood in urine
analgesics
relieve pain
convalescence
recovery time
acute clinical illness
immune response is at its peak and signs/symptoms specific to the disease
prodrome
early, vague nonspecific signs and symptoms
incubation phase
time from exposure to symptoms
nuchal rigidity
stiff neck
photophobia
extreme sensitivity to light
Kernig sign
resistance to extension of leg when hip is flexed
Brudzinksi sign
flexion of the hips and knees in response to neck flexion
host defense failure
failure of the body to mount a response to a pathogen
antigenic variation
pathogens strategies to evade detection
virus hides by going into latency
use immune cells as host to avoid destruction
immunodeficiency
immunodeficiency
inhibit immune components and cells
primary: recurrent severe infections
secondary: results from another disease
hypersensitive reactions
excessive immune response to allergens
atopic
people who develop IgE responses to a variety of allergens
arthus reaction
when a type III hypersensitivity immune complex causes an immune response in the skin that leads to localized necrotic tissues
occurs in lupus and RA
sensitization
phase-first exposure to antigen
memory cells are prodcued
body makes antibodys
elicitation
phase-memory T cells response to a subsequent exposure
allograft
graft between unrelated individuals
trying to obtain a match
autograft
graft/transplant from self or genetically identical individual
autoimmunity
failure to distinguish self from non-self; immune response targets and attacks its own tissues
specific organ damage: type II hypersensitivity antibody mediated
systemic damage: type III hypersensitivity immune complex
alloimmunity
immune response is stimulated in response to the presence of cells from another individual of the same species
kaposi sarcoma
a cancer that causes skin lesion and mucous membrane
unique clinical manifestation in AIDS
Pneumocystitis
fungus growing in the lungs
unique clinical manifestation in AIDS
seroconversion
time from infection to development of antibodies
few weeks up till three months
HIV stage 0
early infection
HIV stage 1
more than 500 CD4 cells/mcL
CD4 = T-helper cells
HIV stage 2
200 through 499 cells/mcL
CD4 = T-helper cells
HIV stage 3
less than 200 cells/mcL
CD4 = T-helper cells
CLASSIFIED AS AIDS
anaphylatic reaction
exaggerated systemic degranulation response
type 1 hypersensitivity reaction (IgE mediated)
degranulation from basophils, neutrophils, eosinophils, mast cells
anaphylatic systemic response:
dilation of vascular smooth muscles (blood vessels)
constriction of bronchial smooth muscle
increase vascular permeability
urticaria
itching hive like reaction
fungi
yeast, molds
protozoa
unicellular organism transmitted via sexual contact, food, water, or insects
malaria, giardia, or trichomonas
atypical bacteria
bacteria with some viral characteristics
mycoplasmas
live on surfaces of host cell
septicemia
when an infection has spread into the blood
sepsis
body’s reaction to septicemia
culture
identifying the presence of microorganisms in tissues (blood) or exudate
sensitivity
identify which antimicrobial drugs would be effective for a pathogen
tinea corpois
body
ringworm
tinea versicolor
skin
hypopigmentation (not a true tinea)
tinea captis
scalp
hair loss or breakage
tinea pedis
feet
maceration between and around toes
tinea cruris
groin
jock-itch, erythema
tinea unguium
nails
nail thickening, discoloration
bronchospasms
difficulty in breathing due to constriction of the smooth muscle in airway
thrush
patches of white infection
located in the mouth
Candida intertrigo
skin fold (under breast) yeast
onychomycosis
yellowing and hardening of nails
located in fingernails
vaginitis
white, cheesy vaginal discharge
located in the proximal vagina
jaundice
yellowing of skin due to excess bilirubin
build up of bilirubin in the skin when the liver can’t efficiently metabolize and excrete bilirubin through feces and urine
antipyretics
drugs that reduce fever
bilirubin
yellow pigment formed during the breakdown of heme in red blood cells
cirrhosis
fibrosis
necrosis
death
hepatitis A
acute
lack of food hygiene, contaminated water, substandard sanitary facilities (awful eating)
vaccine
hepatitis B
acute or chronic
blood and bodily fluids
MOST COMMON
vaccine
hepatitis C
patients can health within 3 to 6 months
acute or chronic
blood to blood
Iv drugs or contaminated medical devices
hepatitis D
blood and bodily fluids
mother to fetus
can only experience when infected with hepatitis B
hepatitis E
fecal oral transmission or contaminated water (awful eating)
lack of food hygiene
hepatocytes
liver cells that can regenerate
kupffer cells
specialized live cells that act to phagocytizes pathogens
help recycle old red blood cells
cellular proliferation
genes, growth factors, nutrients, and stimulation from the external environment
differentiation
the specialization/function of the cell
cellular proliferation and differentiation are under…
the control of genetics
autonomy
excessive cellular proliferation
sense of independence cells become independent from homeostatic control
anaplasia
loss of cellular differentiation
cells have a specific specialization/function
mutator genes
repair DNA and protect genome
disabling the protective DNA repairing mutator gene, the environment is constructed to neoplastic development
proto-oncogenes
code for proteins involved in cell growth and regulation
tumor-suppressor genes
prohibit over proliferation of cells and regulate apoptosis
initiation of cancer
exposure of cells to a carcinogenic agent
causes a mutation in a cell
promotion
a promoter event activates oncogenes
growth and reproduction of mutated cells
promoters: chronic inflammation (increase the proliferation of mutated cells) and environmental chemicals
progression
independent growth
cancerous growth is no longer dependent on exposure to the promoter
neoplastic cells
cancerous cells that ignore normal cellular regulation
proto-oncogenes become oncogenes via:
1.) point mutations
displacement of a singular nucleotide
2.) translocation
chromosomes breaks and relocates
3.) gene amplification
accelerates repilferation of genes
carcinogens (promoter agents)
radiation
hormones
chemicals
tobacco
microbes
cancer must be exposed to an agent!
benign tumors
localized (staying within their region, not passing basement membrane)
resembles tissue of origin
maintains differention, just experiences unregulated growth (hyperplasia)
creates pressure on nearby tissues
contains a capsule
malignant tumors
invasive and destructive
proliferate quickly (goes passed basement membrane)
metasize
does not resemble tissue of origin (lack of differential)
normal count of white blood cells
800 to 3,000 white blood cells CD4 T-cells per mcL
angiodema
swelling towards the face
eyes
mouth
cheek
vectors
organisms that carry the pathogen and pass along
reservoir (have the life cycle)
ticks, mosquitoes, etc.
parasites
obligate (must have host to survive and reproduce)
bacteria
contain cell walls, aerobic, and anaerobic
gram negative: does not have cell wall (no defense mechanism (worse to have an infection off)
gram positive: have cell wall