Lecture 5 Flashcards
General signs/symptoms of infectious diseases
fever, chills, malaise
enlarged lymph nodes
specific S/S for each system
What is the PT role when a pt has an infectious disease?
medical screening
direct treatment
know when to refer out
Aging and immune system
thymus involution, altered T cell-mediated immunity, increased autoantibody production
Infections are ________ in older adults
under-reported
poor historians
absent/poorly localized pain
absence of fever
What are considerations for PT with older populations?
altered mental status
recognize incrased risk of infection
recognize increased risk of AI disease
alert other HCPs of early S/S
Colonization of Organisms
microorganisms present i host tissue, not causing symptomatic disease
person may be a carrier, able to transmit organism to others
Incubation period
period between pathogen entering host and appearance of clinical symptoms
end of incubation period = disease symptoms start
Latent infection
microorganism has replicated, but remains dormant or inactive
Broad categories of pathogens
Viruses
Mycoplasmas
Bacteria
Protoza
Fungi
Prions
Viruses
composed of RNA or DNA nucleus and covered by proteins
can only replicate by invading host cell
extremely difficult to destroy by pharmacological interventions
HIV, herpes
Mycoplasmas
pneumonia
self-replicating bacteria that lack a cell wall
several species are pathogenic in humans
Bacteria
staph, strep
single-celled microorganisms with well-defined cell walls
classified by different properties
Protozoa
Giardia
single celled eukaryotes with cell membranes (not cell walls)
Fungi
Tinea
eujaryotic organisms: digest food externally and absorb nutrients into its cells
mycosis = fungal disease
Prions
Creutzfeldt-Jakob disease, scrapie, BSE
proteinaceous infectious particle
infectious protein structure that converts normal host proteins into abnormally structured form
cause transmissble spongiform encephalopathy diseases, all are untreatable and fata diseases
Chain of transmission
Pathogen
Reservoir
Portal of exit
Mode of transmission
Portal of entry
Susceptible host
Modes of entry
ingestion, inhalation, injection, mucous membrane, transplacental
Portal of exit
area form which pathogen leaves reservoir, usually corresponds to entry into next host
Transmission
contact, droplet, airborne, vehicle, vectorborne
Breaking chain of infection
cleaning and disinfection
Standard and Transmission based precautions
vaccinations
Disease prevention practice for HCPs
Active immunization
handwashing
observer all pts for infection
standard precautions
isolation/transmission based precautions
avoid high risk when you have infection
Standard Precautions
assume all pt blood and bodily fluids are infectious
hand hygiene, respiratory hygiene, PPE, equipment and environmental cleaning
Transmission-based precautions
contact
contact plus
droplet
contact and droplet
airborne
Choosing which product to clean equipment
risk of infection
resistance of pathogen
microbial load
mixed populations
amount of gross stuff present
concetration of pathogen
time/temp
Antiseptics
inhibit microorganism growth & reproduction on inanimate objects, but safe enough to be used on surfaces of living tissue
-static
Disinfectants
inhibit or kill various microorganisms on nonliving objects in environment; should NOT be used on living tissue
ex: micro-kill one germicidal alcohol wipes
-cidal
Sterilization
use of physical or chemical means to kill all microbial life, including highly resistant bacterial endospores (dormant, non-reproductive structures made by a small number of bacteria)
wound care
Spread of C. Difficile
spread by active bacillus or spores
spores –> contact transfer from bad handwashing of HCP (direct). Equipment (indirect)
How can PTs decrease C. Difficile transmission?
Contact plus precautions
Appropriate hand hygiene (alcohol doesn’t kill spores)
Dedicate equipment to pts
STerilize equipment with bleach
Definition of Staph
bacterial genus in 2 groups
aureus, non-aureus
Characteristics of S. aureus
found in environment
can cause skin infections, pneumonia, meningitis, sepsis
#1 cause of nosocomial pneumonia, wound infections
Where are staph found?
found on skin and in anterior nares of healthy people (normal flora)
Bacteremia staph aureus
come from self usually
How is staph spread?
direct and indirect contact
can live on surfaces for 2-6 months
MRSA
s. aureus strain resistant to some antibiotics
Change in MRSA precautions
now doing standard precautions w/history of MRSA
decreases falls, pressure injuries, increases pt satisfaction
Pathogenesis of staph
cannot invade intact skin or mucous membrane
iatrogenic factors
uses exotoxins to detroy host tissue
Clinical Presentation of staph
depends on site of infection
fever, malaise, chills
common in skin, bones, joints, heart valves
Diagnosis and treatment of staph
culture of organism from abscess, drainage, blood
treatment includes drainage and ABX
Prognosis of staph
good with treatment, unless antibiotic strain
Furuncles & carbuncles
infection of skin/subcutaneous tissues by s. aureus
Furuncle
boil, infection of hair follicle and adjacent subcutaneous tissue
hard, painful nodules
local inflammation
purulent exudate
face, neck, armpits, buttocks, thighs
Carbuncle
several furuncles that develop close together, local and deep skin infection
deep abscess, painful, multiple openings
nape of neck/back
Pathogenesis of furuncles/carbuncles
person to person or autoinfection
Treatment of furuncles/carbuncles
topical or oral antibiotics
warm compresses
incision/drainage
Prevention of furuncles/carbuncles
good personal hygiene
Impetigo definition
superficial vesiculopustular infection of skin, found on arms, legs
caused by staph or strep
Transmission of impetigo
HIGHLY contagious
direct or indirect
Risk factors for Impetigo
infants/small children
crowding
multiple skin breaks
poor hygiene
warm, humid weather
skin-skin sports
Presentation of Impetigo
intesne itching and burning (pruritis)
brown sugar legion
face, mouth arms
lymph nodes swelling
Treatment of Impetigo
self-limiting to 2-3 weeks
topical ABX on lesions
antipruritis for itching
do not scratch
Prevention of Impetigo
good personal hygiene
standard and contact precautions
disinfect all pt surfaces
Group A strep (GAS) types
Impetigo
Strep throat
Rheumatic Fever
Necrotizing fasciitis
Group A strep definition
bacteria found in throat and skin
most are mild illnesses, can become severe
Risk factors for GAS infections
chronic illnesses, long term glucocorticoids
Rheumatic fever
acute inflammatory complication from GAS infection
lesions in connective tissues of joints, heart, CNS, subcutaneous
most cases are 5-15 years of age
Pathogenesis of rheumatic fever
in some, follows a previous GAS infection
hypersenitivity type 2 (immune system attack the host)
Long term complcations of acute rheumatic fever
disease–> damage to valves of heart, causes stenosis
death
reccurrent cases due to memory cells
Common presentation of acute RF
polyarthritis
carditits
chorea
Treatment of RF
ABX during, later on for prophylaxis
notify HCPs about history before treatment of other conditions
Pseudomonas aeruginosa
aerobic, motile, gram-negative bacterium
moist environment
grows at 37°
opportunistic pathogen, most common nosocomial
Presentation of Pseudomonas aeruginosa
affect any part of body
progresses raidly to sepsis
sweet, fruity odor
Treatment of Pseudomonas aeruginosa
ABX
surgery for removal of local tissue
HCPS & Pseudomonas aeruginosa
handwashing is most important
clean and disinfect reservoirs (like pools, respiratory equipment)
possibly ABX resistant
Lyme disease
caused by bacterium (borrelia burgodorferi)
transmitted by tick
multisystem disorder
Epidemiology
northeast and midwest
late spring-summer
most prevalent vectorborne infectious disease
Pathogenesis of lyme disease
bacteria lives in mice and squirrels
transmitted via tick
risk is very low if tick is attached for less than 24 hrs
incubation period –> 3-32 days
Diagnosis of lyme disease
history of exposure to ticks and rash
S/S ( the great imitator)
immunoassy –> takes about 2-3 weeks
Initial presentation of lyme disease
bull’s eye rash fadees in 3-4 weeks
behind the knee is common
flu like S/S
Late presentation of lyme disease
intermittent nonerosive inflammatory arthritis
neurologic complications –> bell’s palsy
Treatment
ABX
Prognosis of Lyme Disease
2-4 week course of ABX
anyone can be reinfected
some have persistent symptoms
Post-treatment Lyme Disease syndrome (PTLDS)
completed ABX w/resolution of symptoms, for a new set to return and last for 6 months
pain, fatigue, difficulty concentrating
S/S consistent with fibromyalgia, chronic fatigue
Prevention of lyme disease
reduce exposure to ticks
avoid areas with them
keep them over your skin
check skin, clothes, pets
PT and lyme disease
caution patients to not overuse joints w/arthritis, during flare ups
differential diagnosis is key
make sure to SCREEN for lyme disease
Antibiotic resistance
ability of bacteria to mutate and survive ABX
inappropriate use of ABX causes resistance to occur faster, all ABX use causes selective pressure
happens faster when ABX are used frequently, especially low doses over long periods of time
Common ABX resistant organisms
MRSA
VRE
MDR-TB
MRSA
methicillin -resistant staph aureus
VRE
vancomycin-resistant enterococci
MDR-TB
multiple-drug-resistant mycobacterium tuberculosis
Herpes
8 members of herpes virus family cause human disease
most of us have HSV-1
HSV-1
orofacial infection, usually lips
can affect genitals
50% of us are seropositive at time of puberty
HSV-2
genital infection
painful, watery blisters
can affect face
HSV-4
epstein-barr infectious mononucleosis virus, EBV
mono
Pathogenesis/Transmission of Herpes
via direct skin contact with infected person. Do NOT need symptoms to be infectious
primary infection: enters PNS and moves along axons to sensory gangloa
latency: viral DNA is maintained in sensory neurons
Reactivation: trigger allows virus to travel back down nerves
Triggers for reactivation
stress, increased sun exposure, facial injuries, viral infections, ABX, arginine (chocoalte, peanuts, walnuts)
Clinical presentation of Herpes
prodromes: early symptoms indicting an outbreak will soon happen
HSV 1 = one or clister of fluid filled blisters
HSV 2 = small, painful grouped lesions.
Treatment of Herpes
no cure. immune system destroys active but cannot destroy latent
antiviral drugs
Lysine: supplement commonly used to compete with arginine
Prevention of HSV1 and HSV2
condoms
secual abstinence
antivirals and condoms together
measures to decrease reactivation
Herpetic whitlow
herpes infection around fingernail. occupational risk for HCPs
more common in children, comes from sucking thumbs
unprotected exposure to infected secretions of pt
pain/burning of digit, edema, erythema
wear gloves to prevent
HSV 3
varicella zoster virus
primary VZV infection results in chickenpox
very contagious, childhood disease
VZV remains dormant in CNS, can reactivate to cause shingles
Pathogenesis and Transmission of HSV-3
direct contact with skin sores, indirect contact with contaminated items, droplet, airborne
infected can spread 1-2 days before rash appears
Clinical presentation of chickenpox
headache, low grade fever, malaise, anorexia
rash
serous exudate
Complications of chickenpox
penumonia
enchpahlitis
bacterial infections
reye’s syndrome
Chiceknpox treatment
topicals to relieve itching
pain meds
isolation, cool room
acyclovir –> high risk cases
Shingles
herpes zoster
reactivation of earlier infection
dermatome rash
later symptoms are post-herpetic neuralgia
vaccine available, only PREVENTS, does not TREAT
