Exam 8 (Infectious Disease) Flashcards
Pathogen
Organism or agent that can infect individual causing disease
Virulence
Potency/severity of pathogen
Yersinia pestis kills 50-75%
Candida albicans low risk of serious illness
Colonization
Host is carrying organism but no clinical expression or immune response
Infection
Invasion of pathogen causing immune response
Pathogen evasion
Opportunistic infection
Organism invades host and waits to cause disease till immune system is compromized by something else
Mycoplasm
Smallest bacteria,
Not visible under microscope.
Don’t gram stain
Must use acid-fast to see
Capsule
Hydrophilic gel
Protects cell from immune attack
Helps adhesion
Cell wall
Rigid
Prevents lysis
Provides shape for cell
Gram (+) or Gram (-)
Gram positive cell wall make up
Peptidoglycan with cross linked peptide chains.
Hard to get rid of bc of thick membrain.
Resistant to mammalian enzymes except for lysozime.
Teichoic acids help with adhesion and induces inflammatory reaction
How do we attack gram positive cell clinically
Target peptidoglycan with penicillin.
Blocks peptide cross linking.
Causes cell lysis
Gram negative cell wall make up
Impermeable outer membrane containing lipoplysaccharide endotoxin, phospholipid A, and O antigen.
Periplasm is single layer of peptidoglycan that makes beta-lactamase.
Gram stain
- Crystal Violet
- Iodine (mordant) makes crystal violet hang on
- Acetone or ethanol washes out gram negative
- Saffranin dies gram negative
Acid fast stain
Stain poorly
1. Carbolfuchsin dye (mycolic acid soluble) stains red
2. Organic solvent (acetone or ethanol) extracts stain from non-acid fast
3. Methylene blue stains non acid fast
LPS endotoxin
Gram negative
O antigen
H antigen
Exotoxin
Secreted from bacteria into surrounding body fluids.
Local or systemic
A is pathogen
B is recepto binding facilitating A delivery
C reactive protein
APR
Best lab value to judge treatment response.
Rises within hours of infection.
Takes a week to normalize
Erythrocyte Sedimentation Rate
Rises within 2 days of infection
Can rise 3-5 days after antibiotics initiated
Normalizes in 3-4 weeks
Wet mount
Normal saline to identify cells as pathogens
Potassium hydroxide (KOH) to identify fungi
Dark field microscopy
Identifies syphilis spirochetes
Minimum Inhibitory Choncentration
Minimum amount of ABx to prevent growth after 24 hours of incubation.
Minimum Bacteriocidal Concentration
Minimum concentration of ABx that causes microbial death killing 99.9% of colonies in 18-24 hrs
Blood agar hemolysis
Tests bacteria ability to lyse red blood cells.
Hemolysins.
Alpha is partial
Beta is complete
Gama is none
Coagulase test
Coagulase forms fibrinogen into fibrin to form clot
PCR
Polymerase Chain Rxn
Detects RNA or DNA in viruses
Very specific test.
Amplifies nucleiic acid levels
Antigen testing
Reagent ANTIBODY detects antigens and binds them triggering postive test
Serology
Detect antibody response by measuring antibody levels.
IgM in current or recent infection.
IgG from past infection
In newborns IgM is congenital infection and IgG is just antibodies from mom
Fungus Structure
Thick cell wall of chitin and beta glucan.
Hyphae develop after infection
Spores can be infective
Thermal dimorphism
Spores are infective, not hyphae.
Once in host at body temp fungus grows and becomes infection
Lab testing fungi
Hard to do.
Antigen testing is sensitive and not specific
KOH wet mount
Bacterial medicine target
DORA
DNA
Organelles (lack of nucleus, lack of membrane, 70s ribosomes)
Reproduction
Average size (smaller)
Empiric antimicrobial therapy
Educated guess at best treatment.
Used while waiting on culture to grow.
What influences empiric antimicrobial therapy
Site of infection
Pt history
Local susceptibility data (antibiogram)
Broad spectrum ABx
Work for lots of bacteria.
Saved for emergency situation when pt is going downhill and we don’t know what microorganism is causing it
Saved to avoid causing ABx resistance.
Can alter normal bacteria and precipitate superinfections like C. diff
Bacteriostatic
Stop growth of bacteria
Bacteriocidal
Kill bacteria.
Kill 99.9% in 18-24 hrs.
What to consider with site of infection
Capillaries carrie ABx into tissues.
Capillary permeability varies depending on where at in the body.
BBB
Prostate, testes, and placenta are natural capillary barriers
Lipid solubility of drug.
Size of drug.
Protein binding.
Transporters/efflux pump interaction in CNS
Least toxic ABx
Beta lactams
(ex. penicillin)
Additive risk
Using multiple drugs with same potential toxicities increases risk of pt having that problem
Oral ABx
Appropriate for mild infections
Outpatient
Bioavailability may limit use
Parenternal ABx
For drugs that are poorly absorbed in GI.
Serious infections that require high serum concentrations.
Switch to oral when pt stable
Concentration dependent klling
More effective at higher concentrations.
4-64x MIC
Bolus infusion can achieve high levels of rapid killing
Concentration dependent killing examples
Tobramycin
Azithromycin
Time depending killing dosing
Efficacy determined by percentage of time blood concentration is above MIC.
Used for long time.
Examples of Time dependent killing ABx
Beta-lactams
Clindamycin
linezolid
Post antibiotic effect
Continued suppression of microbial growth even after concentration falls below MIC.
Drugs with long post-antibiotic effect usually only needed once daily
ABx with long post antibiotic effect
Aminoglycosides
Fluoroquinolones
Narrow spectrum ABx
Act only single or limited group of bacteria
Extended spectrum ABx
Effective against G+ bacteria and a good number of G-.
ABx Combination therapy
Single agent is usually best but combonation is useful in certain pts.
Drugs can work really good together but rare (synergism = beta lactams + aminoglycosides).
Some ABx only work if organisms are multiplying.
Can induce resistance
What causes most antibiotic resistance
Genetic alterations of the microbe
Prophylactic use of antimicrobials
Prevention of infection instead of treatment.
Used shortest duration possible
Dental procedures especially if pt has cardiovascular disease.
Surgery to prevent postsurgical infection.
Common ABx after dental procedure preventative
amoxicillin
Common ABx postsurgery preventative
Cefazolin
Vancomycin
Inactivated vaccine
Killed version of pathogen.
Not as strong immunity.
Ex. flu, hep A, rabies
Live-attenuated vaccine
Weakened form of pathogen
Strong, long lasting
One or two doses good for life.
Not good for immunocompromised pts.
Refrigeration required.
Ex. MMR, rotavirus
mRNA vaccine
Inject mRNA for making specific proteins.
mRNA enters human cell and causes protein to be made.
Immune response develops to that protein
Subunit, recombinant, polysaccharide, conjugate vaccines
Uses a piece of specific pathogen.
Strong immune response.
Can be used in immunocompromised.
Boosters may be needed.
Ex. H. flu, Hep B, HPV, Varicella zoster, meningitis, pneumonia
Toxoid vaccine
Contain toxin made by pathogen.
Immune response to toxin.
Booster shots.
Ex. Diptheria, Tetanus
Viral vector vaccine
Uses modified version of different virus as vector for protection.
Johnosn & Johnson COVID-19 pulled from market
Concentration in liquid drugs
Weight of drug per volume
Pediatric antibiotic and antifungal
Usually from dry powder.
Some require refrigeration after mixing
Stable 10-14 days after mixing
Units of dosing
mg of drug/kg of pt
mg/kg/day split that up between however many daily doses
1 kg in lb
2.2 lbs
Incidence
Number of NEW cases in population over certain time
Prevalence
TOTAL number of cases of disease at specific time
Mortality rate
Frequency of death over certain time
Risk
Probability individual in population will develop a disease over time
Clostridium botulinum
Botulism
G+ bacilli
Spore forming
Found in soil
Exotoxin producing
Clostridium botulinum epidemiology
200 annual cases
Foodborne from honey in infants, canned food
Wound botulism IV drug abuse
Clostridium botulin pathogenesis
Toxin taken up in presynaptic terminal.
Acts on SNARE protein inhibiting ACh release into synaptic cleft so muscle can’t contract (flaccid paralysis)
Clostridium botulin clinical findings
Symptoms start 18-24 hrs after ingestion
Inability to swallow
Speech difficulty
Death from respiratory or cardiac arrest
Floppy baby
Clostridium botulin management
ICU
Ventilation
Antitoxins through IV
Botulinum immune globulin
Clostridium tetani
Tetanus
G+ bacilli
Spore forming make it look like tennis racket
Exotoxin producing
Clostridium tetani epidemiology
Rare
Neonatal tetanus
High risk for elderly, diabetics, newborn, unvaccinated mothers, migrants
Clostridium tetani pathogenesis
Spores into body through wound
Spores multiply.
Anaerobic conditions ideal
Necrotic tissue
Makes tetanolysin and tetanospasmin (Low lethal dose)
GABA and glycine blocked by tetanospasmin causing spasms and convulsions
Clostridium tetani clinical findings
Localized tetanus where only one area of body affected is rare.
Generalized tetanus more common
Generalized tetanus
Muscle of face and jaw affected first.
Stiffness
Spasms
Hyperreflexia
Respiratory muscle spasm causing respiratory failure
Opisthotonos posture
Neonatal tetanus
Symptoms at 7 days old
In infants 28 days older or less
From umbilical stump from unvaccinated mother
Tetanus mangement
IM human tetanus Immune globulin within 24 hrs (most important)
Clean wound
Give antibiotics
Keep in calm, quiet environment
Clostridium tetani prevention
Vaccination and boosters every 10 yrs
Infection does NOT confer immunity
Immunization of pregnant women
Yersinia pestis
Bubonic Plague
G- coccobacilli looks like safety pin
Facultative anaerobe
Epizootic
Yersinia pestis etiology
usually rodent to flee to human (arthropod vector).
Then human to human (respiratory droplet).
Can also be directly from rodent (direct)
Prairie dogs and rats
Yersinia pestis mechanism
Capsular Antigen F-1 protects it against phagocytosis.
Lipopolysaccharide exotoxin causes systemic shock and pro-coagulation
V and W antigens
Plasminogen activator allows adhesion to extrcellular matrix proteins
Bubonic plague clinical findings
Incubation 2-7 days.
Sudden onset of severe fever, malais, myalgia, chills.
Large lymph nodes (lymphadenitis)
Septicemic plague clinical findings
Sudden onset of fever, chilld, AMS
Tissue necrosis
Purpuric papules
Pneumonic plague
Incubation is 2-3 days.
From droplet inhalation.
Sudden onset of myalgia, weakness, dizziness
Cough, dyspnea, chest pain
Yersina pestis treatment
Aminoglycosides (streptomycin and gentamicin) are first line
Doxycycline
Chloramphenicol in poor countries
Exposure prophylaxis use fluoroquinolones (levofloxacin, moxifloxacin, ciprofloxacin)
Myobacterium leprae
Leprosy
Hansen’s disease
Acid fast bacilli
Aerobic
Myobacterium leprae epidemiology
mostly in india, Brazil, Indonesia
Happens in second and third decades of life.
Twice as common in men.
Rare in children.
Myobacterium leprae transmission
Human to humans from respiratory droplets.
Myobacterium leprae etiology
2-10 yrs
Only 1-5% of human population susceptible
Myobacterium leprae pathogenesis
Intracellular
In cooler body tissues
Skin
Peripheral nerves (Schwann cells)
Nose, pharynx, larynx, eyes , testicles
Myobacterium leprae Tuberculoid
Strong CMI response
Positive lepromin test
Limited growth
CD4 T cells
Cytokines
INterferon-gamma
Inflmmatory response causes nerve damage
Myobacterium leprae Lepromatous
Pooor CMI response
Negative lepromin skin test
Lesions have lots of bacteria
Infected skin histiocytes
Interferon-beta
Direct contact of organisms causes nerve damage
Myobacterium leprae clinical findings
Myopathy
Neuropathy
Peroneal nerve palsy (foot drop)
Nasal congestion
Epistaxis
Lagopthalmos
Blindness
Myobacterium leprae treatment
Dapsone
Rifampin
Clofazamine
all together
Ebolavirus etiology
Reservoir in fruit bats
Given to humans through contact with bushmeat or apes.
Human to human after zoonotic transmission
Blood born
Reusing needles
Burial of diseased
Ebolavirus pathogenesis
Hepatocyte and endothelial cell damage
Multiorgan failure
Hypovolemic shock
Hypoxia
Hemorrhage.
Ebolavirus cllinical findings
SUdden onset
Fever, chills, malaise, headache
Myalgia
Arthralgia
Maculopapular rash.
SOB
Focal hepatic necrosis
Post ebola syndrome
Recovery takes 7-12 days
Ebolavirus diagnosis
RNA levels peak 7 days after onset.
Early use antigen capture ELISA and RT-PCR
Later use IgM and IgG serology labs
Ebolavirus management
IV fluids
Inmazeb (monoclonal antibodies)
Remdesivir and favipiravir antiviral therapies
Ebolavirus prevention
21 day quarentine
Don’t mess with apes or fruit bats.
PPE
Contact tracing, disinfection, sanitization
Smallpox
Poxviridae family
Linear double stranded DNA virus
8 categories (Orthopoxvirus most important)
Only fully eradicated virus.
Only virus that fully replicates in cytoplasm.
Smallpox pthogenesis
Respiratory droplet inhalation
Spread through lymph nodes
Smallpox clinicla findings
Incubation is 12-14 days
Fever, headache, backache at start.
Lesions erupt over 14-18 days.
All lesions at same stage
Orophayngeal ulceration
Severe systemic. Cold be hemorrhagic and malignant
Smallpox diagnosis
Rule out chicken pox, HSV, VZV first.
PCR.
Vesicular scrapings.
Consult infectious disease and CDC
Smallpox Vaccination
First was live vaccinia virus (cow pox) caused symptoms sometimes.
Second was cloned vaccine used in military
Small pox treatment
No antiviral therapy
Cidofovir may have high activity against poxviruses
Vaccinia immune globulin used.
Poliovirus
Picornaviridae family.
Single stranded RNA
Enterovirus.
Acute flaccid paralysis
Poliovirus etiology
Eradicated in US, but had outbreak in 2022
Poliovirus pathogenesis
Fecal-oral transmission
Viral replication in tonsils and ileum (Peyer’s patches)
Viral dissemination effects peripheral nerve axons and lower motor neurons in the anterior horn.
Poliovirus clinical findings
Incubation is 7-14 days.
90% asymptomatic.
Aseptic meningitis
Can be paralytic or nonparalytic
Postpoliomyelitis happen years later
Paralytic poliomyelitis
Flaccid asymmetric parlysis
Muscle wekaness
Incoordinaition
Painful spasms
Max recovery in six months
Nonparalytic poliomyelitis
Aseptic meningitis
Neck stiffness
Fever
Headache
Rapid and complete recovery
Postpoliomyelitis syndrome
Happens years later.
New onset of weakness and pain.
Progressive muscle limb paresis.
Muscle atrophy.
More common in women
Poliovirus diagnosis
Suggested by aseptic meningitis with acute flaccid weakness and travel to endemic areas
Stool analysis.
CSF analysis.
Lots of diagnoses for acute flaccid paralysis
Poliovirus treatment
No antiviral therapy.
Immune globulin
Respiratory support
Physiotherapy
Poliovirus eIPV vaccine
Inactivated
IM
Trivalent
In US and developed countries
Induces IgA
Poliovirus OPV vaccine
Live, attenuated
Oral administration.
Preferred in eradication efforts.
Don’t give to immunosuppressed
Trivalent OPV associated with vaccine derived polio.
Bivalent better for eradication
Rickettsia prowazekii transmission
Person itches and bacteria from flea (Pediculosis humanus) poop goes inside person.
Flying squirrels have the lice
Rickettsia prowazekii
Epidemic Typhus
Intracellular
G-
Epidemic typhus epidemeology
Uncommon.
Crowded unsanitary regions
Outbreaks in colder months
Epidemic typhus clinical findings
10-14 day incubation
Fever
Cough
Delirium
Rash
Improvement 13-16 days after onset with quick recovery
Myalgia
Arthralgia
Epidemic typhus diagnosis
THrombocytopenia
PCR testing
IgM or IgG serology
Epidemic typhus treatment
Doxycycline (no preg)
Choramphenicol
Borrelia burgdorferi
Lyme disease
Spirochete
Transmitted by deer tick (Ixodes scapularis) that live on deer or mice
Lyme disease epidemiology
Occur more in late spring and summer
Seen more in northeast US
Lyme disease Clinical Findings
Erythema migrans (bullseye)
CN VII palsy
Arthritis
Neuropathy
Encephalitis
ELISA Test
Uses enzyme immunoassay to detect presence of ligand in liquid sample using antibodies against protein being measured
Wester blot
Tests for IgM or IgG.
Hard to tell if infection is current or past
How to test for Lyme Disease
1.ELISA
2. Western blot or second ELISA
How long does tick need to be on person to consider treatment
Between 36 and 72 hours
Give doxycyclin
Lyme disease treatment
1.Doxycycline
2. Amoxicillin
3. Cefuroxime
Rickettsia rickettsii
Rockymountain spotted fever
G-
Intracellular
Rocky Mountain Wood tick and American dog tick
Rocky Mountain spotted fever Epidemiology
Lots in TN.
Length of tick attachment increases risk of transmission.
Most common and severe rickettsial disease
Rocky Mountain Spotted Fever clinical findings
Abrupt symptoms 2-14 days after bite.
Fever
Chills
Headache
RASH.
Vomiting
Myalgias
Restlessness
Rocky mountain spotted fecer diagnoses
Leukopenia
Thrombocytopenia
Hyponatremia
Skin biopsy
Serologic antibody Rickettsia rickettsi IgG
Rocky mountain spotted fever treatment
- Doxycycline even in preg
- Chloramphenicol
West Nile Virus Etiology
Arbrovirus
Mosquitos transmit
Birds give to mosquitoes
Severe neurologic disease
Where is west nile virus
High temps and high rainfall
West nile virus clinical presentation
Incubate for 2-14 days
Only 20-40% symptomatic
NO fever
Maculopaplar rash
Neuroinvasive disease like meningitis, encephalitis, acute flaccid paralysis
West nile diagnosis
IgM antibody-capture ELISA
Plaque reduction neutralization test (PRNT)
Antibodies persist for life so can’t tell if recent or not
West nile treatment
No antiviral meds
Pain control
Dengue virus etiology
Flaviviridae family
Aedes mosquito infect the whole house
Dengue epidemiology
Tropical regions
Second most common mosquito vector borne disease
Dengue clinical finding
ONset 7-10 days after exposure.
Fever
Shock
Bone pain
Thrombocytopenia causing loss of blood.
Dengue diagnosis
Leukopenia
THrombocytopenia
IgM and IgG ELISA
Blood PCR
Dengue treatment
Just pain meds.
NO NSAIDS bc thrombocytopenia
Severe cases need vasopressors and blood transfusion
Zika virus etiology
Flavivirus
Aedes mosquitoes
Spread through Sex
Mother to fetus
Zika virus clinical findings
3-14 day incubation
Often asymptomatic or mild
Zika syndrome
Zika syndrome
Born microcephaly (small head)
Intracranial cerebral malformation
Ocular lesions
Congenital contractures
Hypertonia
Zika diagnosis
PCR early on
ELISA igM after 14 days
Zika treatment
No vaccine or meds.
Just supportive
Most important parasitic disease
Malaria
Malaria etiology
Most important parasitic disease
Plasmodium falciparum from Anopheles mosquito
Malaria clinical findings
Night sweats.
Jaundice
Spleonmegaly
Up to after two months of travel.
Metabolic acidosis
Renal or hepatic failure
Encephalopathy (can cause cerebral palsy, deafnesss, blindness, etc.)
Malaria diagnosis
Giemsa-stained blood smear is best.
Rabpid diagnostic test not as good because won’t test positive for one of the plasmodium species.
PCR used but doesn’t guarantee infection is current.
Trombocytopenia
anemia
Malaria treatment
Artemisnin-based combination therapy (ACT)
Yellow fever
Flavkvirus transmitted by Aedes mosquito
Yellow fever clinical findings
Headache, retroorbital pain, photophobia, bradycardia
Jaundice, hypotension, hemorrhage, delirium
yellow Fever diagnosis
ELISA for IgM
Yellow fever treatment
Supportive
20-50% Mortality.
Vaccination for travelers
Platyhelminths
aka FLATWORMS
Tapeworms (cestodes)
Flukes (trematodes)
Taenia saginata
Beef tapeworm
Taenia solium
Pork tapeworm
Taenia asiatica
Asian tapeworm
Tapeworm treatment
Albendazole or praziquantel
Tapeworm diagnosis
ELISA stool Ag assay
Capsule endoscopy
CSF
Fasciolopsis buski
Intestinal fluke
Effects pigs and humans.
Eggs in snail poop that gets into water and fish.
Eating undercooked fish
Most common in southeast asia
Intestinal fluke diagnosis
Eggs in poop or puke
Intestinal fluke treatment
Praziquantel
Ascariasis
Round worm.
Ascaris lumbricoides.
Poor sanitation
Human feces.
Worms eggs hatch in small intestine then to lungs to grow then back to GI tract to lay eggs.
Ascariasis diagnosis
Eggs and larva in stool
Asariasis Treatment
Albendazole
Pinworms
Nematode (roundworm)
Enterobius vermicularis.
Larva hatch in large intestin.
Females go to anus and lay eggs at night.
Pinworm treatment
Albendazole one now and another a couple weeks later for the whole family.
Wash all bedding and clothing
Hookworms
Ancylostoma duodenale
Necator americanus
Tropical areas.
Itchy foot.
Hook worm clinical findings
Itchy foot.
DIstinct rash on foot (looks like a worm)
Cough during lung migration.
Hookworm diagnosis
Eggs in stool.
Iron deficiency.
hemocult
Hookworm treatment
Albendazole
Hookworm prevention
Mass treatment of children in endemic areas
Pasteurella multocida
Gram negative coccobacilli
Transmitted by dog and cat bite (30-50% of cat and 5% of dog)
Pasteurella multocida clinical findings
Bite or scratch
Symptoms 3-24 hrs after bite
Soft tissue infection
Bone and joint infection
Respiratory infection
Bacteremia
Osteomyelitis
Septic arthritis
Endocarditis
Meningitis
Pasteurella multocida clinical diagnosis
Wound cultures
Radiograph
Pasteurella multocida management
Wound debridement and irrigation
Amoxicillin-clavulanate (augmentin)
DO NOT suture
Bartonella henselae
CAT SCRATCH FEVER
G- bacilli
Bartonella henselae clinical findings
Brown or red papule/ulcer at site of injury
Painful lymphadenopathy
Splenomegaly
Eyes mess up
Neurology problems
Found in immunocompromised
Bartonella henselae diagnosis
Serology
Lymph node biopsy
PCR
Bartonela henselae management
Self limited
Azithromycin first line
Doxycyclin or azithromycin and rifampin(ocular and neuro) for severe.
Francisella tularensis
TULAREMIA
G- coccobacillus
Virulent
Grade A bioterrorism
Rabbits
Tick or insect bites around rabbits
Inhalation
Tularemia pathogenesis
Hematogenous spread
Spreads in lymph
Kill macrophages and spread
Tularemia clinical findings
Sudden onset after 3-5 days.
Splenomegaly
Fever
Papule or ulceration at site
GI involvement
Meningitis
Pericarditis
30-50% hospitalized
Main type of tularemia
Ulceroglandular
Tularemia diagnosis
Serology
PCR
Antibodies to F. tularensis
Measure at symptom onset and two weeks later
Tularemia managament
- Streptomycin
Lyssavirus
RABIES
Rhabdovirus family
Highest fatality of infectious disease
From animal bite (mostly bats)
Rabies pathogenesis
Transmitted by saliva.
Replicates in peripheral tissues
Enters nervous system
Disseminates salivary glands and replicates
Rabies clinical findings
80% cephalic
Once symptoms start its too late.
Delerium
Hydrophobia
Aerophobia
Autonomic instability
20% paralytic causing coma and death (from respiratory failure)
Rabies diagnosis
Nigri bodies in brain.
FLuorescent antibody testing
PCR
What to do after bite when suspecting rabies
Clean wound
Give immunization
Give immunoglobulin time of exposure
Give vaccine on days 0 3 7 14
Both if pt never had vaccine
Don’t give imunnoglobulin if been vaccinated
Hantavirus
HEMORRHAGIC FEVER
Enveloped RNA bunyavirus
Aerosol inhalation of contaminated soil with urine and feces.
From field mouse and deer mouse
35-40% mortality
Hantavirus clinical findings
Hemorrhagic fever with renal syndrome
Flu-like
oliguria
diuresis
Hantavirus cardiopulmonary syndrome
Pulmonary edema
Vascular leakage
Hantavirus diagnosis
Serology
ELISA for igG and igM
Reverse PCR
Autopsy testing for viral N antigen
Hantavirus treatment
Supportive care
Renal support
Ribavarin (antiviral)
Chlamydia psittaci
PSITTACOSIS
PARROT FEVER
G- cocci
Inhalation of bird feces
Psittacosis clinical findings
Rapid onset after 5-10 days
Flu like symptoms
SOB
Dry cough
Encephalitis
Respiratory failure
Psittacosis diagnosis
CXR
Serology is best
Rales/crackles in lung
Pleural friction rub
Hepatosplenomegaly
Psittacosis management
Tetracycline and doxycycline first line
Macrolides second line or for kids
Brucella melitensis, abortus
Brucellosis
G- coccobacilli
Ingestion of unpasteurized milk or cheese
Meat from cattle, hogs, goats
Brucellosis clinical findings
Fever
Sweating
Odor
Weight loss
Weakness
Endocarditis
Meningitis
Miscarriage
Brucellosis diagnosis
Bone marrow culture is best
Blood or urine culture also used
ELISA for IgM and IgG
Brucellosis management
First lineis doxycylclin for 6 weeks followed by Rifampin
Brucellosis relapse
Most occur in first three months
Brucellosis prevention
Vaccinate livestock
Milk pasteurization
Bacillus anthracis
ANTHRAX
G+ rod
aerobic
spore forming
Sheep wool (Woolsorter’s disease)
Anthrax clinical finding
Cutaneus is papule vesicles and Ulcerations
Inhaled is viral-like illness and sepsis
GI is bloody emesis, constipation, diarrhea Mortality is 85%
Anthrax diagnosis
Culture from cutaneous lesions or blood.
PCR testing
Microscopy with grams stain
CXR
Mediastinal widening
Hemorrhagic lymphadenitis
Anthrax management
Ciprofloxacin for cutaneous.
Ciprofloxacin + meropenem + minocycline + raxibacumab for systemic (2 bactericidal, 1 protein synthesis, 1 RNA synthesis inhibitor)
Coxiella burnetti
Q FEVER
G- coccobacilli
Aerosolized inhalation of spores, dust droplets
From feeces, urine, parturition material of goats, cattle, sheep
Ingestion of raw milk
Q fever clinical findings
Febrile
Pneumonia
Endocarditis
Aortic aneurism
Increased incidence of lymphoma
Pregnancy problems
Q fever management
Doxycycline
Duration depends on presence of native valve vs prosthesis
Q fever prevention
Milk pasteurization
Detect infection livestock
Toxoplasma gondii
TOXOPLASMOSIS
Parasitic infection
TORCH infection
Congenital infection that effects fetus
Toxoplasmosis trasmission
Contact wit cat feces, undercoooked meat or contaminated soil
Tranplacental
Toxoplasmosis clinical findings
Can be asymptomatic
Nontender bilateral, symmetrical cervical or diffuse LAD
AMS
Focal neurologic problems
Eye pain
Chorioretinitis
ToxoplasmosisToxoplsamosis diagnosis
Serology
Test for IgG and IgM
Toxoplasmosis management
Pyrimethamine and sulfadiazine
For pregnant use Spiramycin to reduce risk of transmission
What patients are normally effected by toxoplasmosis in CNS
Pts with AIDS bc low CD4 T cells
Encephalitis
Chorioamnionitis
dissemiated disease
MRI
Giardia lamblia
GIARDIASIS
Parasitic infection from dirty water.
Giardiasis clinical findings
Acute noninflammatory diarrhea for possibly over 3 weeks.
Abd pain
Malobsorption
50% of pt go chronic
Giardiasis diagnosis
Stool exam for eggs of parasitess
Stool antigen assay
Giardiasis management
Tinidazole first line
Metronidasole
Virus strain
When variant comes very unique from other strains it is considered another strain.
Not all variants are strains
All strains are variants
Alpha covid
First variant
More deadly than original
Beta covid
South Africa in 2020
More transmisible than original strand but not many cases in US
Gama covid
Japan and brazil in 2020
Not much around now
Delta covid
India 2020
Highly transmissible.
More severe in unvaccinated
Spreads faster
Omicron covid
South Africa 2021
Currently circulating
>98% of cases since 02/2022
When was covid not health emergency anymore
May 5, 2023
Covid mode of transmission
Respiratory droplets.
Covid symptoms
Respiratory
Neurologic (confusion)
GI issues
What people were effected by covid worse
Blacks
Hispanics
Males
Elderly
Physical exam findings of covid
Diaphoresis
Dry mucous membranes
Tachycardia
Tachypnea
Crackles or rhonchi
Wheezing
Abd tenderness
Lower extremity pain or edema
What labs to order for someone with covid symptoms
CMP
CBC
ABG
CXR
Strep test
Flu test
RSV screen
COVID test
What O2 sat do we keep covid pts at
At least 94%
Covid lab findings
Neutrophilia
Lymphocytpenia
Thrombocytopenia
Elevated bilirubin
Elevated D-dimer
High fibrinogen
Elevated con Willebrand factor
coagulopathy
Standard to diagnose covid
PCR
Imaging for suspected covid
CXR
Head CT
Chest CT
Doppler ultrasound of lower extremities to rule out DVT
Chest CT and Xray early on
Could seem normal
What meds to not start covid pts on but if they are already on it continue meds
NSAIDS
ACEi/ARBs
Statins and aspirin
Nebulizers with covid pts
Don’t give nebulizer because risk of infection through respiratory droplets
Only drug approved by FDA against COVID
Remdesivir
200mg IV on day 1 then 100 mg IV for next four days
Don’t give if GFR<30
Can be given to anyone as long as weigh atleast 1.5kg
What drug is given to covid pts with respiratory failure and are on oxygen
Dexamethasone (decadron) (a steroid)
Significantly lowered mortality.
Not useful for pts with no respiratory issues
Plasma use in covid
Not recommended anymore.
Didn’t do any good
Case by case for pediatric
Tocilizumab
IL inhibitor (antiinflammatory)
Can’t be given with Baricitinib
Don’t give if underlying bacterial pulmonary infection
Baricitinib
JAK Inhibitor (antiinflammatory)
Helps in children with covid that require oxygen.
Give with dexamethasone
Can’t be given with Toxcilzumab
Don’t give if underlying bacterial pulmonary infection
Anticoagulants approved for pediatrics
Unfractioned heparin
Low molecular weigh heparin
Warfarin
Rivaroxaban
Dabigatran
Deep vein thrombosis
Inflammatory labs to check
Procalcitonin
Ferritin
Erythrocyte sedimentation rate
C-reactive protein
D-dimer
Lactate dehydrogenase
Fibrinogen
Troponin
Creatine phosphokinase
Acute respiratory distress syndrome
Lung tissue widespread injury that diminishes ability to get enough oxygen
Lung issues from covid
Pulmonary fibrosis
Pneumomediastinum
Subcutaneous emphysema (rice crispies)
Pneomothorax
Outpatient meds for covid
Nirmatrelvir (paxlovid)
Developed by Pfizer
Metallic taste side affect
Helps prevent long covid
First oral antiviral against covid
Molnupiravir.
Reduces time to recovery, but doesn’t work that good.
Second choice after paxlovid
Multisystem inflammatory syndrome in children
Occurs in <1% after covid.
Macrophage activation syndrome
Cytokine releases syndrome
Usually occurs 6-8 weeks after covid.
GI
Rash
Respiratory
Neurocognitive
Red or swollen lips
Strawberry tongue
Kidney injury
Lymphadenopathy
Swollen hands and feet
Hepatitis
Myocardial dysfunction
How to treat Multisystem inflammatory syndrome in children
IV immunoglobulin
Glucocorticoids (IV methylprednisolone)
TNF inhibitors, IL 1 and 6 inhibitors
Common complications of covid
Cardiovascular
Kidney
Death
Seizures
Stroke
Memory loss
Depression
How old do you need to be for covid vaccine (mRNA)
12
6 months-11yrs for only emergencies
Common side effects of Moderna and Pfizer vaccine
Endocarditis and pericarditis at first
Overall benefits outweigh risk
Long covid
Symptoms continue for at least three months
Contamination
Bacteria is there but not replicating
Critical colonization
Replicating bacteria with no invasion but affecting wound healing
Staphylococcus aureus
Methicillin resistant is MRSA
G+
Healthcare associated MRSA
Infection over 48 hrs from hospitalization or within 12 months of care exposure.
Makes biofilm on foreign devices like tracheal tube orcatheter.
Community associated MRSA
Skin and soft tissue infections in young, healthy individuals outside of hospital.
Sharing needles
Sports
Prisons
Military
Group A. Streptococcus
S. pyogenes
Pharyngitis
Skin
Soft tissue (non-necrotizing) tissue
Group B Streptocci
S. agalactiae
Neonatal sepsis/meningitis
Sepsis
in GI and GU tract
Groups CFG streptococci
Bacteremia
Endocarditis
Septic arthritis
Group D streptococci
Associated with clononic malignancy
Endocarditis
Hepatobiliary disease
Enterococcus
G+
In GI of humans and animals
E. faecalis
E. faecium
Enterococcus risk
Indwelling catheters
Cardiovascular abnormalities
Prolonged hospitalization
Mechanical ventilation
ABx use
Immunodeficiency
Vancoomycin-resistant enterococci
G+
Hospital acquired
Colonize in GI
Live for 5-7 days on counter
24 hours on bed rails
60 mins on phone
30 mins on stethoscope
Vancomycin-resistant enterococci ris
ABx use
ICU for 72 hours
Underlying medical problems
Clostridium
Rod shaped bacilli
G+ anaerobes
C. perfringens
Gas gangrene
Food poisoning
Supportive vare treatment
Clostridial gas gangrene
C. perfringens
Subcutaneous gas
Traumatic wound, post-opp, or spontanious in immunocompromised or intestinal disease
Pseudomonas aeruginosa
G- aerobic bacillus
In water
Prefers immunocompromised host
“no flowers in the burn unit” - Dr. Beck
Pseudomonas aeruginosa pathogenisis
Some strains just in lungs causing cystic fibrosis.
Some invade tissues causing pneumonia or bacteremia leading to septic shock and death.
Pseudomonas aeruginosa soft tissue infections
Sweet smell
Green
Ulcers
Malignant otitis externa
Escherichia coli
G- bacillus
Normal in GI tract
Isolated from stool cultures
GU infections causing cystitis, pyelonephritis, prostatitis, abdominal infections, pneumonia, meningitis
Cellulitis
Grup A strep (pyogenes)
Usually unilateral lower extremities.
Indistinct borders
Can become bullous or necrotic
Cellulitis predisposing factors
Skin trauma
Inflammation
Edema from lymphatic drainage or venous insufficiency.
Obesity
Cellulitis treatment if MRSA present
Trimethoprim/sulfamethoxazole or amoxicillin
Cellulitis treatment if MRSA not present
Dicloxacillin, cephalexin, or cefadroxil
Cellulitis treatment in immune compromised
IV Cefazolin, naficillin, or oxacillin for Immune compromised
Stasis dermatitis
Very similar to cellulitis symptoms
Raise leg above heart, if redness goes away, it is stasis dermatitis
Eryspelas
Beta-hemolytic streptococci
Involves upper dermis and superficial lymphatics.
Usually unilateral
usually lower extremities
Erysipelas nonpurulent
Clear border
Milian’s ear sign
Erysipelas ad cellulitis labs
Draw with marker around area to see if grows over time.
No labs needed or diagnosis, just physical exam
Erysipelas treatment
Penicillin V potassium
Amoxicillin
Cephalexin
Cefadroxil
Erysipelas treatment for high risk or immunocompromised
Cefazolin
Nafcillin
Oxacillin
Skin abscess
Colllection of puss in dermis or subcutaneous space
Usually S. aureus (can be MRSA)
Painful
Spontaneous drainage can occur
Skin abscess treatment
Incision and drainage
Culture drainage for anaerobic/aerobic bacteria.
Give antibiotics that cover MRSA (trimethoprim-sulfamethoxazole, doxycycline, minocycline)
Large abscess needs IV therapy after.
Don’t pack wound
Treatment for abscess followed by sepsis
Vancomycin and cefepime or Meropenem
Carbuncle
Made up of furuncles.
Usually S. aureus.
most common presentation of MRSA
Furuncles are firm, tender, red nodules
Carbuncles larger
Furuncle and carbuncle treatment
Incision and drainage
Culture of drainage
Trimethoprim-sulfamethoxazole, doxycycline, minocycline
IV vancomycin or daptomycin if septic
Severe sepsis needs vancomycin and cefepime or meropenem
Folliculitis
Inflammation of hair follicle.
Usually infectious
Staph aureus most common (MRSA possibly)
Follicular pastules and inflammed papules
Folliculitis barbae
Bacterial folliculitis of hair follicles of beard and face
Hot tub folliculitis
Pseudomonas aeruginosa
Folliculitis diagnosis
Pt history and physical exam.
Gram stain
KOH for fungal
Folliculitis treatment if MRSA suspected
Doxycycline
Trimethoprim-sulfamethoxazole
Clindamycin
Persistent folliculitis treatment
Dicloxacillin
cephalexin
Impetigo
Direct bacterial invasion or infection at skin trauma.
Usually staph aureus
Could be Strep A
Nonbullous impetigo
most common impetigo
Lesions to papules
Thick honey crust
Mild impetigo treatment
Mupirocin or retapamulin
Extensive impetigo treatment
Dicloxacillin
Cephalexin
Impetigo treatment with penicillin allergy
Erthtomycin or clarithromycin
Impetigo treatment if MRSA suspected
Doxycycline
Trimethoprim-sulfamethoxazole
Clindamycin
Type I soft tissue infection
Polymicrobial
Aerobic or anaerobic
Co-morbidities at older ages
Type II necrotizing soft tissue infection
Monomicrobial
Group A-hemolytic strep or
Staph. aureus
Necrotizing myositis
Very rare
Blunt trauma or heavy exercise
Necrotizing cellulitis
Anaerobic pathogens
How to diagnose and treat necrotizing soft tissue infections
Surgical exploration.
Surgery needed in 24 hours
Amputation may be necessary
CT scan gas seen from bacteria
In OR gas can be heard from bacteria eating
Broad spectrum ABx
Clostridial myonecrosis
Gas Gangrene
Necrotizing infection
Traumatic is Clostridium perfringens.
Spontaneous is Clostridium septicum
Traumatic clostridial myonecrosis clinical manifestation
Sudden onset of pain at trauma site.
May appear pale then bronze then red/purple
Crepitus in soft tissue
Gas in deep tissues seen in CT
Tramatic clostridial myonecrosis labs
Blood and tissue cultures
CBC
CMP
Large Gram variable rods at injury
Traumatic clostridial myonecrosis treatment
Surgical debridement.
Antibiotics that cover clostridium and group A strep
Same for spontaneous
Spontaneous clostridial myonectosis
Clostridium septicum
GI tract
Neutropenic pts
GI lesion allows it into blood.
Purpleish fluid
Direct specimen
Pathogeni localized in sterile site
Surgical or needle aspiration
CSF, liver, lung, blood
Indirect specimen
Pathogen localized but must pass through site containing normal flora to be collected
Sputum or urine sample
Mixed sample
Sample site with normal flora.
Throat and stool
Susceptible
Organism inhibited by serum concentration of drug using usual dosage
Intermediate
Organism inhibited by only maximum dosage
Resistant
Organism resistant to achievable serum drug levels
What to consider when choosing ABx
Efficacy
Cost
Side effects
Resistance
Drug availability at site of infection
Class I wound
Clean wound with no iflammation
Mostly closed
Class II wound
Clean-contaminated
Class III wound
Contaminated
Open, fresh, accidental
Class IV wound
Dirty/infected
Old traumatic would with stuff inside
When should prophyalctic antimicrobial therapy start for surgery
60 minutes before surgery
When to discontinue prophylactic antimicrobial therapy for surgery
24 hrs after surgery
