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Gram Staining Classification
based on cell wall structure
NOT disease severity
Gram-Positive Bacteria
thick peptidoglycan layer
no outer membrane
retains crystal violet
stains purple
Gram-Negative Bacteria
thin peptidoglycan layer
outer membrane with lipopolysaccharide (LPS)
loses crystal violet
strains pink with safranin (counterstain)
Gram-Negative Triggers…
stronger inflammatory responses
endotoxins
harder to treat and leads to serious infections
sepsis and shock
Sepsis
harmful response to an infection
causes inflammation that can damage organs
Shock
inflammation from sepsis causes blood vessels to leak and widen
Early Gram Staining
help guide empiric antibiotic therapy while awaiting cultures
cannot use once antibiotics are given
bacteria may not show up
Empiric Antibiotics
broad spectrum antibiotic
given before culture comes back
Culture Time Frame
takes 24-72 hours
possibly longer
Sensitivity Testing Purpose
determines which antibiotics:
kill the organisms (susceptible)
are ineffective (resistant)
initial treatment
Culture Purpose
identifies the specific organisms
used for specific antibiotic treatment
Nurse’s Role in Cultures and Sensitivities
ensuring proper specimen collection technique
monitoring for clinical improvement or worsening
understanding C&S helps nurses explain why antibiotics change mid-hospitalization
How Resistance Occurs With Bacteria
mutation
changes during DNA replication
gene transfer
bacteria swap genetic material, allowing resistant genes to spread
can spread across species
How Bacteria Adhere to Host Tissues
pili/fimbriae attach to mucosal surfaces
(ex. E. coli in the urinary tract)
first step in infection
mechanical flushing helps prevent infection
Mechanical Flushing Examples
urination
coughing
sneezing
diarrhea
vomiting
Where Bacteria Adhere to Host Tissue
mucous membranes
urinary tract cells
intestinal walls
tissue surfaces.
Exotoxins Defintion
secreted proteins that directly damage host cells
both Gram-negative and Gram-positive bacteria produce
Endotoxins
part of Gram-negative LPS
released upon bacterial death
causes fever, hypotension, DIC, septic shock
Toxin Production Nursing Relevance
patient’s fever, hypotension, or altered mental status in infection = systemic toxin effects, not just local inflammation
altered vital signs = problem
Biofilm Definition
formation protects bacteria from antibiotics
(device infections often require device removal)
Where Biofilm Occurs + Why
medical devices
urinary catheters
IV lines
pacemakers
teeth (dental plaque)
mucosal surfaces (gastrointestinal and respiratory tracts)
likes moist environments and synthetic surfaces
Opportunistic Infection
normal flora takes advantage of weakened immunity or disrupted barriers
high-risk: elderly, immunocompromised, post-surgical
Local vs Systemic Bacterial Infection Presentation
Local: change at a specific site
edema, erythema, warmth
cellulitis, wound infection
Systemic: affects the body
vital sign alteration
sepsis, shock
How to Know Patient is Responding to Antibiotics
symptom resolution
monitor temperature
WBC
cultures
C. Diff Organism
Gram-positive, spore forming, anaerobic bacillus
C. Diff Pathophysiology
disrupts normal gut flora
(most often by broad-spectrum antibiotics)
spores germinate in the colon
activates toxin A (enterotoxin) and toxin B (cytotoxin)
C. Diff Spreading
spreads by pores
contact isolation
alcohol hand sanitizer is ineffective
soap and water is required (mechanical)
C. Diff Symptoms
watery diarrhea
dehydration
electrolyte imbalance
abdominal pain
fever
can progress to toxic megacolon
Toxic Megacolon
life-threatening
colon is inflamed/paralyzed
colitis: colon inflammation, nothing is moving
rupture
shock
Toxic Megacolon Signs
abdominal distention
absent bowel sounds
rebound tenderness
(pain after palpation)
Treatment of C. Diff
oral vancomycin
fidaxomicin
NOT anti-diarrheal medications
Pneumonia Pathophysiology
causes alveolar inflammation and fluid
leads to impaired has exchange
hypoxia
Pneumonia Symptoms
fever
productive cough
dyspnea
crackles
consolidation on chest x-ray
(exudate - RBCs, WBCs, bacteria)
Antibiotics for Pneumonia
start empirically
narrowed after cultures
Pneumonia Nursing Relevance
early mobility (mucus)
incentive spirometry to aid clearance
monitor O2
monitor sputum color
vaccination education
Streptococcus Organism
Gram-positive cocci in chains
Streptococcus Causes
throat, skin, and lung infections
pharyngitis (strep throat)
scarlet fever (rash)
Post Streptococcal Complications
can trigger immune-mediated complications after the infection resolves
Post-Streptococcal Glomerulonephritis
caused by a type III hypersensitivity reaction
not active infection
kidney disease
hematuria, edema, hypertension
Staphylococcus Organism
Gram-positive cocci in clusters
Staphylococcus Causes
skin infections
abscesses
build up of pus
sepsis
MRSA
reistant to beta-lactam antibiotics
requires alternative therapy
Food-Borne E. Coli Symptoms
severe abdominal cramping
bloody diarrhea
E. Coli Warning
can lead to:
hemolytic uremic syndrome (HUS)
acute kidney injury
E. Coli Nursing Relevance
AVOID antibiotics
can worsen toxin release
give supportive care
monitor urine output
notify provider if bloody stool
C. Botulism Toxin MOA
blocks acetylcholine release
causing descending paralysis
and respiratory failure
C. Botulism Symptoms
neurologic symptoms
diplopia (double vision)
dysphagia (difficulty swallowing)
little or no fever
Staphylococcal Food Poisoning Caused By
pre-formed toxin
leading to rapid, onset vomiting
Gonorrhea + Chlamydia Defintion
STI
transmitted through unprotected vaginal, anal, or oral sex
may be asymptomatic
Untreated Chlamydia + Gonorrhea
at risk for:
pelvic inflammatory disease (PID)
infection of the female reproductive organs
infertility
ectopic pregnancy
fetus develops outside the uterus
Chlamydia and Gonorrhea Screenings
based on sites of sexual contact
not assumed anatomy
Syphilis Stages
Primary: painless chancre (ulcerated skin lesion)
Secondary: immune → rash on palms/soles
Latent: organism dormant (no visible symptoms)
Tertiary: chronic inflammation
organ damage
Syphilis Screening
blood screening test (PRP or VDRL)
“reactive” titer may need titer result to look for active infection
history of syphilis → always has reactive RPR
Nursing Key Role in Infection Control
medication timing
patient education
prevention of resistance
Sepsis
life threatening response to an infection
occurs when the immune response becomes systemic and dysregulated
not the infection itself
Sepsis Inflammation Causes
widespread vasodilation
capillary leak
Sepsis Vasodilation Leads to
hypotension
poor tissue perfusion
a critical reduction in blood flow, oxygen, and nutrients to body tissues
lactic acidosis
leads to shock, organ failure, or death.
Sepsis Capillary Leak Causes
third spacing
edema
Early Signs of Sepsis
hypothermia
tachycardia
tachypnea
labs:
elevated lactate
abnormal WBC
Late Sign of Sepsis
hypotension (dangerous)
Septic Shock
sepsis can rapidly progress to septic shock
defined by persistent hypotension despite fluids
vasopressor needed (constricts blood vessels)
Sepsis First-Line Treatment
IV resuscitation
rapidly administering fluids
restore lost volume, improve blood pressure, and ensure vital organs get oxygen
antibiotic therapy
Bacteriostatic
interfere with the cell’s ability to reproduce
Bactericidal
actively kill bacteria