Fever Flashcards
what conditions are classified as immunocompromised
cancer, organ transplantation, diabetes, renal failure, cirrhosis, asplenism, HIV, etc.
components of innate immunity
physical barriers: intact skin, GI and respiratory mucosa, cilia, biofilm, gastric acid, antibacterial substances in pancreatic and biliary secretions, antimicrobial peptides and proteins on skin and mucous membranes and resident microflora
initial inflammatory response: sentry cells detect pathogens and release cytokines
reticuloendothelial system: tissue macrophages and monocytes - encapsulated organisms
what type of bacteria does reticuloendothelial system target
encapsulated organisms- pneumococci, meningococci, and H. flu
components of adaptive immunity
humoral immuniry: antibodies, Igs, complement
cell mediated immunity: T lymphocytes, NK cells, and mononuclear phagocytes
what are the different subtypes of Ig
IgM- first to appear - acute
IgG- chronic, 75%of Ig mass, crosses placenta
IgA- Ig in GI fluids, nasal and oral secretions, tears and other mucous fluids
IgE- on mast cells/basophils, immediate type hypersensitivity reactions
what immune deficiency should be tested for in people with meningococcemia
complement deficiency - may benefit from immunization
what bacteria are people with complement deficiency susceptible to
S. pneumoniae, H. flu, Neisseria meningitidis and Neisseria gonorrhea
what medication condition is associated with complement defieciyn
SLE
what bacteria /viruses/funguses are people with cell mediated immunity deficiencies susceptible to
Mycobacterium tb, listeria, salmonella, MAC, legionella, nocardia
DNA viruses: CMV, HSV, and HZV, EBV, measles, adenovirus
fungus: Candida, Cryptococcus, Mucor, Aspergillus, and Pneumocystis, Histoplasmosis, Coccidiodies
protozoa: Toxoplasma gondii
parasites: cryptosporidium, strongyloides stercoralis
how to differentiate between margination of neutrophils during periods of stress or with increased catecholmaines/steroids with infection
infection has increased immature bands whereas margination is increase mature neutrophils only
bacteria people with splenectomy or asplenia susceptible to
S. pneumo H. flu N. meningitidis Capnocytophaga canimorsus Bordetella holmesii
parasites: Babesia
bacteria people with neutropenia are susceptible to
GN bacilli: E. coli, Klebsiella, Pseudomonas, Enterobacter, Serratia, Citrobacter, Proteus, Acinetobacter, Stenotrophomonas
GP cocci: Staph epidermis, Staph aureus, Viridans streptococci, Strep pneumo, Strep pyogenes, Enterococcus
GP rods: corynebacteria, bacillus
fungi: candida, aspergillus, .. less common: mucor, rhizopus, trichosporon, fusarium, pseudallescheria
define neutropenia
neutrophil count less than 500 cells/mL or 0.5 x 10^6 cells
or less than 1.0 x 10^6 and expected to drop to 0.5 x 10^6
define febrile neutropenia
single T of 38.3 in neutropenic patient or T of 38.0C or higher during 1-2 hours
most common sites of infection in neutropenic patients
lung -25% mouth and pharynx -25% GItract - 15% skin, soft tissue and intravascular catheters - 15% perineum and anorectal area - 10% UTI - 5% nose/sinuses 5%
risk factors for serious viridans streptococcal infections
aggressive cytoreduction for acute leukaemia or allogeneic bone marrow transplantation, profound neutropenia, and severe oral mucositisi
prophylactic use of TMP-SMX or fluoroquinolone, used of antacids or H2 blockers and childhood
in patient with neutropenia, ulcerative lesions in the mouth suggestive of
viridans streptococci, HSV, Candida, anaerobes
in patient with neutropenia, necrotizing skin lesions
Pseudomonas aeruginosa, Aeromonas hydrophily, Aspergillus, Mucor
in patient with neutropenia, nontender, subcutaneous nodules
nocardia, cryptococcus
in patient with neutropenia, nontender pink skin papules
candida
in patient with neutropenia, black eschar of nose or palate
aspergillus, mucor
in patient with neutropenia, generalized macular red rash
viridans streptococci
in patient with neutropenia, RLQ abdo pain, tenderness, distension, bloody diarrhea
typhlitis (neutropenic enterocolitis) caused by pseudomonas, e coli, clostridium septicum
in patient with neutropenia, perineal pain and tenderness without inflammation or abscess
GN bacilli, anaerobes
in patient with neutropenia, redness or pain at vascular catheter sits
coagulase negative staphylococci, corynebacterium, bacillus species
what factors make pt with febrile neutropenia high risk for complications
patients with hypotension, pneumonia, new onset abdominal pain, neuro changes, other acute organ dysfunction (especially renal or hepatic disease, active COPD)
how to calculate MASCC score in febrile neutropenia (multinational association for supportive care in cancer)
burden of febrile neutropenia with mild or no sx.
no hypotension (SBP > 90)
no COPD
solid tumor or heme malignancy with no previous fungal infection
no dehydration requiring parenteral fluids
burden of febrile neutropenia with moderate symptoms
outpt. status
age younger than 60 years old
what empiric IV abx to use in febrile neutropenia
anti-pseudomonad beta-lactam (cefepime, meropenem, imipenem-cilastatin, or pip-tazo) ASAP after cultures obtained
add amino glycoside or Vanco for hypotension
may add azithro for pneumonia
if suspected polymicrobial/anaerobic ie. intraabdominal or perianal source - ad flagyl or clindamycin if cefepime is used as the beta-lactam agent
what abx to use for febrile neutropenic in pen-allergic patietns
minor allergy- cefepime, meropenem, or imipenem-cilastatin
severe allergy: consult ID, aztreonam and Vanco +/- clinda or flagyl
when to use vancomycin empirically in febrile neutropenia
suspicion of serious catheter-related infection, known colono=ization with MRSA or penicillin resistant pneumococci, known isolation of a GP organism before final identification and susceptibility known, presence of shock, severe mucositis, prior fluoroquinolone prophylaxis, and institutions in which MRSA, VRE and strep mitis are frequent pathogens
when to consider urgent CT scanning in febrile neutropenia
CXR normal or inconclusive in pt with acute respiratory symptoms/signs, HRCT chest without contrast
facial pain or swelling is present, consider CT scan of sinuses without contrast
in patients with abdominal pain and tenderness, CT abdominal pelvis with IV contrast
what patients make up high risk group of febrile neutropenia
inpatient when fever and neutropenia develop, presence of comorbid medical conditions, uncontrolled cancer, acute leukaemia, hemodynamic instability, evidence of organ failure, presence of pneumonia, severe soft tissue infection, infection of a central line, abdominal pain, or neuro or mental status abnormalities, neutropenia expected to last more than 10 days
considerations for outpatient management of febrile neutropenia
pt should have MASCC score > 21
pt medically stable without acute or chronic organ dysfunction or comorbid conditions, and no acute leukaemia
no focus of infection identified
pt has access to telephone and transportation to return to hospital 24 hours a day and has a caregiver at home
p that hx of compliance with f/u
pt not on fluoroquinolone prophylaxis
pt oncologist agrees to outpatient mgmt
should give IV dose in ED and watch for 4 hours before D/C
outpatient abx used in febrile neutropenia
cipro or levofloxacin PLUS clavulin or clinda (in pen allergy patients)
DDX of fever in non-neutropenic patents with solid organ cancer
wound infection, deep abscess, or perforated viscus
infections in central venous or urinary catheters, steps, and prosthetic devices
large tumor lesions can cause obstructive infections (of bronchus, bile duct, or ureter)
treatment of suspected meningitis in immunocompromised host - LIsteria
ampicillin and gentamicin
septra in pen allergic
hyponatremia + pneumonia symptoms in immunocompromised patient is
Legionella
treatment of legionella infection in immunocompromised patietns
reso fluoroquinolone or azithromycin
clinical manifestations of nocardia
subacute pneumonia with nodular infiltrates
cellulitis
subcutanoeus abscesses
meningitis brain abscess
treatment of nocardia
sulfonamides + other agents
presentation of Stronglyloides
intestinal nematode in patients with deficient CMI and usually on high dose steroids
disseminates from intestine to lung and other organs causing Strongyloides hyper infection syndrome with v. high mortality - wheezing, cough, SOB, hemoptysis sand hemorrhagic rash are common
treatment of sStronglyoides
oral ivermectin
DDX for pulmonary infiltrates - diffuse/ bilateral in immunocompromised patietn
viral: CMV, RSV, influenza, adenovirus, varicella
pneumocystis jiroveci
fluid overload/pulmonary edema
TRALI
radiation damage
chemotherapy-induced toxicity
ARDS due to viridans streptococcal bacteremia
bronchiolitis obliterates
pulmonary hemorrhage
progression of disease (lymphangitic spread, leukaemia infiltrates)
DDX for pulmonary infiltrates- focal or patchy in immunocompromised patients
bacterial pneumonia including legionella fungi: invasive pulmonary aspergillosis, zygomycosis, fusarium, pseudallsecheria tb non-tb mycoabcteria nocardiosis PE
factors contributing to diabetic increased risk of infection
defects in immune function
excess glucose for fungal/bacterial growth
vascular insufficiency related to microangiopathy and atherosclerosis
sensory neuropathy leads to wound neglect
infections more commonly seen in diabetics
rhino cerebral zygomycosis malignant otitis externa - Pseudomonas pneumonia caused by S.aureus and GN bacilli tb emphysematous cholecystitis UTI Fournier's gangrene/ nec fasc of lower extremities psoas abscess spinal epidural abscess foot infections with osteomyelitis post op surgical site infections vulvovaginal candidiasis
factors contributing to immunocompromised state in alcoholism and cirrhosis
alcohol suppresses the immune system, alters blood flow, depresses metal status and delays care-seeking
more likely to aspirate
alcoholic cirrhosis: deficient hepatic clearance and killing of bacteria by reticuloendothelial cells, and splenic hypo function; complement deficiency since liver makes C3, cellular immune deficiency occurs and is exacerbated by malnutrition, bactericidal activity of IgM decreased
what infections are cirrhosis patients more susceptible to
spontaneous bacteremia and sepsis caused by E.coli, Klebsiella, Salmonella, streptococci, Vibrio vulnificus, and Aeromonas
SBP caused by E.coli, K. pneumoniae, S.pneumo, or enterococci
pneumonia caused by pneumococci, GN bacilli (E. coli, klebsiella, H.flu) and anaerobes
tb
meningitis by S. pneumonia, listeria
skin/soft tissue with S.aureus, streptococci, and GN bacilli
factors contributing to immunocompromised state in renal failure
disruption of cutaneous barrier at vascular access sites, etc.
uremic prurituswith excoriatoin/skin breakdown
reduced renal clearance of toxins, nutritional deficiencies, and administration of immunosuppressive medications
CKD leads to generalized immune hyporesponsiveness
common infections seen in renal failure
vascular access site infection by S.aureus - may cause hematogenous spread - often osteomyelitis seeding ribs or thoracic vertebrae, endocarditis, meningitis, epidural abscess, septic arthritis
SBP
what conditions cause functional asplenism
sickle cell disease, ulcerative colitis, celiac disease, sarcoidosis, amyloidosis, RA and SLE
what can be seen on peripheral smear that may indicate functional hyposplenism
Howell-Joly bodies in RBCs
complications of prolonged steroid use
Cushing’s syndrome, PUD, pancreatitis, benign intracranial hypertension, psychosis, glaucoma, poster sub capsular cataract, poor wound healing, sodium retention, hypertension, vascular thrombosis, hyperglycaemia, DKA, HHS, AVN of bone, myopathy and osteoporosis, adrenocortical insufficiency
patients taking biologics at risk for what infections
reactivation of late tb, non-tb mycobacterial infection, histoplasmosis, and coccidiomycosis
cryptococcosis, listeriosis, legionellosis, salmonellosis, aspergillosis, candidiasis and pneumocystosis
DDX of fever -infectious
resp: bacterial pnuemonia, PTA, retropharyngeal abscess, epiglottiti, OM, sinusistis pharyngitis, bronchotiis, influenza, tuberculosis
CV: endocaditis, pericarditis
GI: peritonitis, appendicits, cholecystitis, diverts, colitiis or enteritis
GU: pyelonephritis, TOA, PID, cystitis, epidydimitis, porostatitis
skin: cellulitis, infectd deucubitus ulcer, soft tissue abscess
systemic: sepsis or septic shock, meningococcemia
DDX of fever- noninfectious
critical diagnoses: MI, PE, ICH, CVA, NMS, thyroid storm, acute adnreal insufficiency, transufion rxn,, plmonary edema
emergent: CHF, dehydration, recent seizure, sickle cell disease, transplant run, pancreatitis, DVT
nonemergent diagnoses: drug fever, malignancy, gout, sarcoidosis, crohn disease, postmyocardiotomy syndrome
considerations when fever associated wit bradycardia
pt on beta blockers etc.
factitious or drug related fevers
typhoid fever, brucellosis, leptospirosis
rheumatic fever, lyme disease, viral myocarditis, endocarditis
suspect case of diphtheria
pharyngitis, nasopharyngitis, tonsillitis, larnygitis, tracheaitis, absent or low grade fever
greyish adherent pseudo-membrane present
membrane bleeds, if manipulated or dislodged
probable case of diphtheria
suspect case plus one or more of following:
stridor
bull-neck (cervical edema)
toxic circulatory collapse
acute renal insuffieincy
submucosal or subq petechiae
myocarditis
death
recent return (<2 weeks) from travel to endemic area
recent contact (<2 weeks) with confirmed case or carrier, or visitor from area with endemic diphtheria
recent contact with dairy or farm animals or domestic pets
immunizaiton status
lab confirmed case of diphtheria needs
positive culture of Corynebacterium diphtheria or Corynebacterium ulcers AND
positive Elek test or PCR for tax gene (positive for subunit A and B)
DDX of respiratory diphtheria
streptococcal pharyngitis viral pharyngitis (EBC, adenovirus, HSV) tonsillitis vincent's angina (typically involve gingiva whereas dip doesn't) acute epiglottitis mononucleosis laryngitis bronchitis tracheitis Candida albicans rhinitis
bacteria causing diphtheria
Corynebacterium diptheriae
what category of bacteria is diphtheria
gram positive bacillus
unencapsulated
pathophysiology of diptheria
toxin strains of C.diphtheria lysogenized and produce an exotoxin that inhibits cellular protein synthesis
diphtheria membrane composed of leuks, RBCs, fibrin, epithelial cells and bacteria results from necrosis caused by local effects of the exotoxin
exotoxin causes peripheral neuropathy manifested by muscle weakness - pharyngeal usually affected first, then proximal muscles
emergent complications of diphtheria
airway obstruction, CHF, cardiac conduction abnormalities and muscle paralysis
diagnostic w/u of suspected diphtheria
notify lab because routine cultures don’t ID organism
Elek test -tests for toxin A
PCR - used to detect toxin structural gene
mgmt of diphtheria
equine serum diphteria antitoxin
active immunization
erythromycin 40mg/kgk/day in divided doses
pen G 300,000U /day in those weighting 10kg or less, or 600,000U/day in divided doses
admit, isolate and monitor for detection of arrhythmias
how is diphteria transmitted
resp droplets or direct contact with secretions, skin lesions, fomites on food
how is pertussis transmitted
droplet
bacteria that causes pertussis
Bordetella pertussis
pathophysiology of pertussis
adheres to ciliated respiratory epithelial cells, releases several toxins
systemic effects of pertussis toxin = sensitization to lethal effects of histamine and increased excretion of insulin (hyperinuslin, therefore hypoglycaemia)
clinical case of pertussis defition
cough and illness for more than 2 weeks with no apparent other cause plus one of: paroxysms of coughing, inspiratory whoop, post-jussive emesis
probably case of pertussis
clinical case defn
not lab confirmed
not epidemiologically linked to a lab confirmed case
confirmed case of pertussis
acute cough illness of any duration with positive culture for B. pertussis
clinical case defn + confirmed by PCR
clinical case defn + epidemiologically linked to case confirmed by culture or PCR
clinical course of pertussis
incubation period: 7-10 days
catarrhal/prodromal phase: 1-2 weeks, rhinorrhea, low fever, malaise, conjunctival injection
paroxysmal phase: begins as fever subsides, cough worsens 1-10 weeks
convalescent phase: residual cough
complications of pertussis
periorbital edema subconjunctival hemorrhage petechiae epistaxis hemoptysis subcutaneous emphysema pneumothorax pneumomediastinum diaphragmatic rupture umbilical and inguinal hernias rectal prolapse pneumonia
diagnostic w/u of pertussis
NP aspirate or swab for culture and PCR
DDX of pertussis
acute viral URTI, pneumonia, bronchiolitis, cystic fibrosis, tb, AECOPD, FB aspiration, leukemia (marked leukocytosis)
treatment of pertussis
O2, suctioning, hydration, nutrition, avoid respiratory irritants
admit if: associated pneumonia, hypoxia, CNS complication, or severe paroxysms, kids under age 1
abx to decrease infectivity and carriage
erythromycin, or azithromycin (day 1 -10mg/kg, then day 2-5 - 5mg/kg)
prophylaxis for household contacts
alternative to treat pertussis in macrolide allergic patietn
septra
what kind of bacteria is pertussis
gram negative coccobacilli - aerobic
what kind of bacteria is tetanus
spore-forming, motile, rod-shaped obligated gram positive anaerobic bacillus
what is the bacteria name for tetanus
Clostridium tetani
pathophysiology of tetanus
portal of entry required - tetanus prone wounds have damaged or devitalized tissue, foreign bodies or other bacteria - wound, OM, foreign bodies, corneal abrasions, childbirth, dental procedures
C. tetani produces neurotoxin that causes clinical illness
tetanospasmin binds motor nerve ending blocks presynaptic release of GABAergic and glycinergic neurons
what are the 4 types of clinical tetanus
generalized tetanus
localized tetanus
cephalic tetanus
neonatal tetanus
clinical manifestations of generalized tetanus
trismus, rictus sardonicus, irritability, weakness, myalgies, muscle cramps, dysphagia, hydrophobia, and drooling
autonomic dysfunction causes death - tachycardia, htn, hyperpyrexia, cardiac dysrhythmias, and diaphoresis
clinical manifestations localized tetanus
persistent muscle spasms to site of injury
clinical manifestations of cephalic tetanus
rare variant of localized tetanus resulting in CN palsies and muscle spasms
clinical manifestations of neonatal tetanus
generalized tetanus in newborn due to inadequate maternal immunization and contaminated material used to cut/dress umbilical cord
complications of tetanus
acute respiratory failure form respiratory muscle spasms
autonomic dysfunction
forceful tetanic muscle spasms can cause vertebral subluxations and fractures, long bone fractures, joint dislocations
rhabdomylosis
secondary infection
DVT/PE - prolonged immobility
hyperthermia
GI: peptic ulcers, ileus, intestinal perforation, and constipation
SIADH
diagnostic w/u in tetatnus
cultures not helpful
check calcium to r/o hypocalcemia
spatula test: tough oropharynx with tongue blade- positive = reflex masseter muscle spasm
DDX for tetanus
strychnine poisoning - antagonizes glycine release, but doesn’t block GABA like tetanus does
acute abdomen black widow spider bite dental abscess/infection dislocated mandible dystonic reaction encephalitis head trauma hyperventilation syndrome hypocalcemia meningitis PTA progressive fluctuating muscle rigidity (stiff-man syndrome) psychogenic rabies sepsis status epilepticus SAH TMJ syndrome
treatment of tetanus
aggressive supportive care: benzos, avoid unnecessary stimulation (causes more spasms), NM blockade and MV if cannot control
elimination of unbound tetanospasmin: HTIG
active immunization: Td
prevention of further toxin production: flagyl 500mg q6h
contraindication to Tdap vaccine
hx of neurologic or severe hypersensivity reaction to previous dose
what wounds need Tdap and TIG in ED
pt with unknown or less than 3 primary vaccine series- - clean wound: Tdap only, other wounds: Tdap + TIG
pt with 3 vaccine series previously: clean wound- if less than 10 years since previous give Tdap, other wounds- if less than 5 years since previous give Tdap
what types of wounds are high risk for tetanus
> 6 hours old, > 1cm deep, contaminated, stellate, denervated, ischemic, infection
what is the bacteria that causes botulism
Clostridium botulinum
what are the five types of botulism
food-borne botulism, infant botulism, wound botulism, unclassified botulism and inadvertent botulism
what kind of bacteria is C. botulinum
anaerobic, gram positive, rod-shaped organism
clinical manifestations of food-borne botulism
early symptoms: weakness, malaise, lightheadedness, N/V, and constipation
neuro sx: diplopia, blurred vision, dysphonia, dysphagia, dysarthria, and vertigo –> symmetric descending muscle weakness - neck muscles, UE > LE
-blocks cholinergic receptors so get dry mouth, ileum, urinary retention
-ocular: ptosis, EOM palsies
clinical presentation of infant botulism
constipation, poor feeding, weak cry, loss of head control, hypotonia, CN palsies, ocular invovlement
differences in wound botulism
GI symptoms absent
incubation period longer 4-14 days
toxin produced by spores in wound
diagnostic tests in botulism
diagnosis confirmed by detection of toxin in blood
notify public health
serial measurements of patients vital capacity
DDX botulism
pharyngitis/gastroenteritis initially
GBS (usually starts distal and ascends, paresthesias can be present)
tick paralysis (ascending, lack of bulbar involvement)
myasthenia gravis (eye signs also prominent, but pupil response preserved, no autonomic symptoms)
poliomyelitis- fever, asymmetrical neuro signs, CSF abnormalities
Eaton-Lambert- avoids bulbar muscles usually
brainstem CVA- acute onset, asymmetrical
anticholinergic toxins
organophoste insecticides
dystonic reactions
heavy metal poisoning
Mg toxicity
paralytic shellfish poisoning
DDX infant botulism
sepsis viral illness dehydration encephalitis meningitis failure to thrive GBS, MG, polio hypothyroid hypoglycemia diphtheria toxin exposures inborn errors of metabolism congenital muscular dystrophy cerebral degenerative diseases
treatment of botulism
supportive care, admit to ICU as respiratory failure may develop rapidly and insidiously
antitoxin
consider bowel decontamination
infant botulism with - BabyBIG - pooled plasma from immunized adults with high titters of antibodies to toxins
if using abx for secondary infection don’t use aminogylcosides or tetracyclines because they impair Ca entry to neuron and can worsen effects of the toxin
what infections does Strep pneumonia cause
OM, pneumonia, meningitis,
less common: endocarditis, septic arthritis, and peritonitis
what populations are at higher risk of pneumococcemia (Strep pneumoniae in the blood)
chronic resp or CV disease, chronic EtOH abusers, patients with cirrhosis, diabetes mellitus, or an absent or functionally impaired spleen, those receiving immunosuppression, those with CRF, nephrotic syndrome, organ transplant, lymphoma, Hodgkin’s disease, multiple myeloma, and AIDS
what kind of bacteria is Strep pneumo
encapsulated gram positive facilitate anaerobe
what lab findings correlate with more serious disease in pneumococcemia
normal or low WBC count
hypoxemia and hypercarbia
treatment of Strep pneumo positive blood cultures
penicillin G 2-4 million units IV q4h
ceftriaxone 2g IV daily
treatment of pneumococcemia in penicillin allergic or cephalosporin allergic patients
vancomycin, imipenem, chloramphenicol
what is the mortality rate of meningococcemia
40%
70% if septicemia without meningitis
less than 10% if only meningitis
bacteria that causes meningococcemia
Neisseria meningitidis
what kind of bacteria is N.meningitidis
aerobic gram negative diplococci
encapsulated
what are the 5 patterns of presentation of N.meningitidis infection
occult bacteremia meningococcal meningitis meningococcal septicaemia fever and non blanching rash chronic meningococcemia
what is the rash seen in meningococcemia
purpura fulminans
complications of meningococcemia
acute respiratory failure
renal failure
meningitis- focal neuro deficits, seizures, hearing loss, visual deficits, neurodevelopment impairment, CN palsies, hemi and quadriparesis
purpura fulminans - loss of digits or limbs from gangrene
purulent or immune complex arthritis and pericarditis
herpes labialis
poor prognostic indicators in meningococcal disease
WBC less than 500, platelets less han 100, metabolic acidosis, purpura fulminans, onset of petechiae within 12 hours of admission, absence of meningitis, presence of shock, low sedimentation rate, and extremes of age
DDX of meningococcal disease
viral exanthema rocky mountain spotted fever typhus/typhoid fever endocarditis vasculitis syndromes (PAN, HSP), toxic shock syndrome, acute rheumatic fever dengue fever drug reactions ITP TTP
empiric therapy for meningitis
corticosteroids prior to abx decreases long term neuro sequelae in adults and children (not true for neonates), dexamethasone 0.4-0.6mg/kg/day q6h for 4 days
ceftriaxone 100mg/kg IV followed by daily doses of 100mg/kg in divided doses q12h
+vanco
+/- ampicillin
clinical case definition of toxic shock syndrome
fever: t >38.9
rash: diffuse macular erythroderma
desquamation 1-2 weeks after onset of illness, particularly palms/soles
hypotension
multisystem involvement: 3 or more of the following:
GI: V/D
muscular: severe myalgia or CK level 2x ULN
mucous membrane: veginal, oropharygnal, or conjunctival hyperemia
renal: BUN or Cr at least twice ULN or urinary sediment with pyuria in the absence of UTI
hepatic: total bili, AST, and ALT at least 2x ULN
hematologic: platelets < 100
CNS: disorientation or alterations in consciousness without focal neuro signs when fever and hypotension are absent
lab criteria:
negative results:
on blood, throat, CSF cultures (blood culture may be positive for Staph aureus)
rise in titer to RMSF, leptospirosis or rubeola
probable vs confirmed case of toxic shock
probable: lab criteria met and 4/5 clinical findings present
confirmed: lab criteria met and 5/5 findings including desquamation unless pt dies before desquamation occurs
case definition of streptococcal toxic shock syndrome
hypotension
multisystem involvement: 2 or more of the following
-renal: Cr > 177 or 2 x ULN
-heme: platelets < 100 or DIC
-hepatic: total bili, AST and ALT 2x ULN
-ARDS
-generalized erythematous maculopapular rash that may desquamate
-soft tissue necrosis, including necrotizing fasciitis, myositis or gangrene
what bacteria can cause toxic shock
staph aureus
group A streptococcus
risk factors for toxic shock syndrome
use of superabsorbent tampons post-op wound infections postpartum period nasal packing cancer common bacterial infections ethanol abuse infection with influenza A infection with varicella virus diabetes mellitus HIV chronic cardiac disease chronic pulmonary disease NSAID use
what are some differences with staphylococcal and streptococcal toxic shock syndrome
sex: staph more common in women, strep equal
severe pain at site of infection: common in strep, rare in staph
erythroderma rash: more common in staph\
bacteremia: low in staph, 60% in strep
tissue necrosis: rare in staph, common in strep
predisposing factors: tampons, packing, NSAID use in staph; cuts, burns, bruises, varicella, NSAID use in strep
mortality rate: <3% in staph, 30-70% in strep
clinical manifestations that prompt consideration of toxic shock syndrome
patients with fever, rash, hypotension, evidence of end-organ function such as respiratory failure or AMS
prodromal illness of fever, chills, N/V, watery diarrhea, h/a, myalgia and pharyngitis can last 2-3 days before frank sepsis
rash- nonpruritic, diffuse, blanching, macular erythroderma
-strep TSS may have scarlet-fever like rash- petechiae, maculopapular lesions, mucosal- strawberry tongue, mucosal ulceration; conjunctival/scleral hemorrhages
-mental status abnormal out of proportion to degree of hypotension
complications of TSS
ARDS, shock, gangrene, DIC, neuropsych problems, renal failure irreversible in 10%
rhabdo, seizures, pancreatitis, pericarditis, cardiomyopathy
menstrual form may reoccur
lab abnormalities in TSS
leukocytosis or leukopenia elevated Cr hypoalbuminemia and life threatening hypocalcemia anemia, thrombocytopenia prolonged INR and PTT increase bill elevated transaminases metabolic acidosis pyuria elevated CK
DDX for toxic shock syndrome
any septic illness with exanthema, heat stroke, cellulitis, Kawasaki disease, staphylococcal scalded skin syndrome, scarlet fever, drug reactions -SJS, TEN, RMSF, clostridia gas gangrene, leptospirosis, meningoceoccemia, gram negative sepsis, atypical measles, and viral illnesses
treatment of toxic shock syndrome
fluid resus - may need 10-15L/day supplemental O2 monitored setting remove source- tampon, nasal packing etc. surgical consult to debride wounds vasopressors pre abx: clindamycin 1st line 600-900mg IV q8h IVIG if suspected strep
4 categories of transplant organ complications
anatomy
rejection
infection
drug toxicity
what are the subtypes of anatomic complications of organ transplant
vascular: thrombosis, stenosis, AV fistula, pseudo aneurysm formation nonvascular anastomosis (ie. bile ducts, bronchi, ureters): leaks, obstructions from scarring, migration of stent, stone development complications related to surgery
three phases of organ rejection / what occurs at each
hyperacute: preformed antibodies against MHC or ABO blood type antigens
acute: days to weeks after transplant, constitutional symptoms and signs of transplant organ insufficiency (or anytime later if immunosuppression is stopped)
chronic: months to years, gradual failure of transplanted organ over time, ie. interstitial fibrosis/tubular atrophy in kidneys, inflammation causing airway obstruction in lungs, fibrosis of bile ducts, veins and arteries in liver, CAV - chronic allograft vasculopathy
infectious pathogens in transplant patients 0-1 months post-transplantation (early)
pre-existing in transplant patient: bacterial colonization (Pseudomonas aeruginosa, M. tb), viral (HIV, HBV, HCV, CMV, HSC, VZV), fungal (Candida, Cryptococcus neoformans, Aspergillus, Histoplasma capsulatum, Blastomyces dermatidis, Coccidiodes immitis)
donor-derived: bacteria from transplant bacteremia, fungal (Candida species), rarely Trypanosma cruz, HCV, HIV, West Nile virus, lymphocytic choriomeningitis virus, Legionella, H. capsulate, Strongyloides stercoralis, C. neoformans, Schistosoma species, Toxoplasma gondii, and M. tb
nosocomial: bacteremia, surgical site infection, VAP, UTI, C.diff, MRSA, VRE, resp viruses, Legionella
infectious pathogens in transplant patients 1-6 months post-transplant (intermediate)
viral infections: CMV, EBV, HBV, HCV, BK virus, respiratory viruses, HSV, VZV
opportunistic infections: Listeria monocytogenes, Nocardia, C.neoformans, Mycobacterium species, Candida species, Aspergillus, H. capsulatum, B. dermatitis, C.immitis, Pneumocystis jiroveci, T.gondii, S. stercoralis
infectious pathogens in transplant patients more than 6 months post-transplant (late)
community acquired pathogens: respiratory viruses, community-acquired pneumonia, UTI
chronic viral infection: CMV, EBV, HBV, HCV, BK virus
opportunistic infections: in patients remaining on high dose immunosuppression
presentation of CMV infection in transplant patients
may be asymptomatic
fever, malaise, and leukopenia or symptoms specific to invasive disease of lungs, liver or GI tract
lungs: fever, hypoxia, diffuse infiltrates on CXR
liver: microabscesses in liver
GI: abdo pain, diarrhea, bleeding, perforation
effects of CMV on transplant patients unrelated to infection
immune-modulating properties, increased risk of bacterial and fungal infections, opportunistic infection, acute or chronic organ rejection, increased mortality
linked with glomerulopathy and graft dysfunction in renal allograft recipients, recurrent HCV in liver transplant, acute cardiac dysfunction and accelerated atherosclerosis in heart transplants
how to treat CMV
IV ganciclovir
often patients are on prophylaxis of valganciclovir for 3-6 months
effects of EBV infection on transplant patients
mononucleosis like syndrome: fever, malaise, pharyngitis, lymphadenopathy or hepatitis, pneumonitis, and GI complaints
post-transplant lymphoproliferative disorder: viral mononucleosis syndrome, plasmacytic hyperplasia, B-cell infiltration of organs, or lymphoma
treatment of post-transplant lymphproliferative disorder
reduction in immunosuppression, monoclonal B-cell antibody therapy (rituximab), cytotoxic chemotherapy
how does BK virus present in post-transplant patients
resides in kidneys, can progress from viruria to viremia to nephropathy, graft dysfunction and graft loss in renal transplants
how does Listeria infection present
immunocompetent: fever, abode pain, diarrhea
immunocompromised: bacteremia, meningoencephalitis
treatment of Listeria in solid organ transplant patients
high dose pen or amp + aminoglycoside
which organ transplant patients have highest incidence of Nocardia
heart/lung
presentaiton of Nocardia
fever, cough, SOB, hemoptysis, but can progress to disseminated infection with CNS abscess, skin and soft tissue abscess
what does Nocardia look like on culture
classic beading and branching gram positive bacilli
what is first line treatment for Nocardia
septra
what are secondline/other optinos to treat Nocardia
minocycline, amikacin, imipenem, cefotaxime, ceftriaxone
how does invasive candidemia in transplant patients present
fungemia, UTI, peritonitis, pleural empyema, IAI
how does aspergillosis present in transplant patients
pulmonary nodules w/ or w/o cavitation, may disseminate to any organ system including CNS
treatment for aspergillosis
amphotericin B, azoles or echinocandins
what are examples of endemic mycoses
histoplasmosis, blastomycosis, and coccidiomycosis
how to treat endemic mycoses in organ transplant pt
amphotericin B
treatment of Pneumocystis jiroveci
septra + steroids depending on degree of hypoxia
presentation of toxoplasmosis
usually reactivation of latent infection - causes pneumonia, HSM, myocarditis, brain abscess, or diffuse encephalitis
treatment of toxoplasmosis
IV sulfdiazine and pyrimethamine
septra has been used to treat toxo in AIDS pts successfully
what is the presentatino of cryptococcus neoformans in solid organ transplant patients
meningoencephaltiis
1/3 have lesions on imaging
how to diagnose cryptococcus neoformans
LP or serum cryptococcal antigen
amphotericin B and flucytosine
what happens when transplant patients develop primary varicella
life threatening with pneumonia, pancreatitis, hepatitis, encephalitis, and DIC
treatment of primary varicella in transplant pt
varicella zoster Ig
IV acyclovir
presentation of Stronglyoides stercoralis in transplant patients
intestinal nematode causing hyperinfeciton syndrome causing necrotizing hemorrhagic enterocolitis and hemorrhagic pneumonia
disseminated Stronglyoides causes severe abdominal pain, obstructive symptoms, hemorrhage, and secondary peritonitis, sepsis, meningitis, and pneumonia
treatment of disseminated Strongyloides
thiabendazole
what are typical prophylaxis abx. post transplant
septra (for pneumocystis, but also covers Nocardia, Listeria, and UTIs)
fungal prophylaxis with fluconazole
CMV prophylaxis with ganciclovir
3 categories of patients with infections from 1-6 months post transplant
healthy transplant: no chronic immunomodulating viral infections and a functioning allograft- mild increased susceptibility to normal community acquired infections, such as flu, UTI, pneumococcal pneumonia
chronic viral infection: progressive disease- HBV, HCV cause liver dz, HCC; EBV -> PTLD; CMV after prophylaxis stopped; HSV reactivation
chronic rejection: require ongoing high dose immunosuppression, highest risk for life-threatening opportunistic infections, and standard nosocomial infection
toxicity associated with cyclosporine
nephrotoxicity, hypertension
tremor, hyperkalemia, hyperuricemia, glucose intolerance, hyperlipidemia, hirsutism, GI upset, gingival hyperplasia
toxicity associated with tacrolimus
nephrotoxicity, neurotoxicity (tremor, h/a)
hypertension, hyperlipidemida, glucose intolerance, GI upset, hypokalemia, alopecia
toxicity associated with sirolimus
nephrotoxicity, impaired wound healing, pneumonitis
hyperlipidemia, edema, GI upset, anemia, stomatitis
toxicity associated with azathioprine and mycophenolate mofetil
hepatotoxicity, bone marrow depression, GI upset
toxicity associated with prednisone
glucose intolerance, osteoporosis, GI bleeding, myopathy, cataracts
adverse effects on induction agents- monoclonal antibodies ie. basiliximab, muromonab-CD3 (OKT3)
increased risk opportunistic infections, PTLD
pulmonary edema in overhydrated oliguric patients
aseptic meningitis
which drugs interact with cyclosporine, tacroliums and sirloumus by decreasing half-life and immunosuppressive effect, and cause potential for acute rejection
carbamazepine, nafcillin, phenobarbital, phenytoin, rifampin
which drugs interact with cyclosporine, tacroliums and sirloumus by increasing the half-life and potential drug toxicity or immunosuppression
colchicine, diltiazem, fluconazole, fluorquinolones, ketoconazole, macrolides, oral contraceptives, verapamil
which drugs interact with cyclosporine, tacroliums and sirloumus to cause increased nephrotoxicty
aminoglycosides, amphotericin B, cimetidine, NSAIDs, sulfur
differences in cardiac physiology post heart transplant
resting heart rate 95-110 - loss of PNS tone
meds affected autonomic NS- ie. atropine have no effect ton heart
pressers work by increasing catecholamines
no classic anginal symptoms due to lack of innervation
heart sensitive to adenosine, half dose
ECG changes after heart transplant
incomplete RBBB and depolarization abnormalities most common
bi-atrial technique: may demonstrate two P waves (one from native recipient sinus nose and one from donor sinus node)
what to do with pt with heart transplant with symptomatic bradycarda
admit, may need pacemaker
what to do with pt with heart transplant with new tachyarrhythmias
concerning for rejection or CAV ( cardiac allograft vasculopathy)
how does acute rejection present in cardiac transplan tpatients
fatigue, fever, dyspnea (most sens), signs of HF, hypotension
pericardial effusions, atrial arrhythmias.
w/u of heart transplant pt when considering rejection
ECG, CBC, lytes, Cr, troponin, cultures, CXR, echo
what is the gold standard for diagnosing acute rejection in heart transplant
endomyocaridla biopsy
treatment of acute rejection in heart transplants
IV corticosteroids with or without OKT3 or ATG
if Ab mediated rejection, plasmapheresis, IVIG with rituximab
how to diagnose chronic allograft vasculopahty )CAV)
angio - diffuse concentric narrowing coronary arteries (vs. eccentric focal narrowing in classic cardiac atherosclerosis)
most common in diction for liver transplant
HCV infection
what is the most common vascular complication of liver transplant
hepatic artery thrombosis
presentation of hepatic artery thrombosis
in 1st month post liver transplant- jaundice, RUQ pain, fever, elevated liver enzymes and bili
how to diagnosis hepatic artery thrombosi
Doppler ultrasound, helical CT scan or arteriography
anatomic complications of liver transplant
hepatic artery thrombosis
hepatic artery rupture: usually caused by bacterial arteritis
biliary complicatiosn: leask, obstruction, stricture
how to diagnose rejection of liver transplant
biopsy
what infections are common in liver transplant patients
adominal/biliary infections ie. cholangitis, peritonitis, liver abscess, and abdominal abscesses
most common- GN bacilli, enterococci, anaerobes
staph, candida can also occur
invasive aspergillosis
HBV, HCV
what is anatomic location of transplanted kidney usually
iliac fossa
clinical manifestations of kidney graft rejection
fever, hypertension, edema, tenderness over the allograft, and decreased urine output, subtle rise in Cr
anatomic complications in lung transplant
PTX, hemothorax, pleural effusion, empyema, persist air leak
clinical manifestations of acute rejection in lung transplant
fews days to several years after transplnt
cough, dyspnea, fatigue, fever
rales and rhonchi heard with deterioration in oxygenation and pulmonary function
what is the most common opportunistic infection in lung transplant and when is highest risk
3 weeks to 4 months
CMV pneumonia
howt o differentiate between rejection and CMV infection in lung transplant
transbronchial biopsy and culture
difference n organ transplant patients in trauma
give leukorediced and CMV negative blood
heart transplant patients may have clinical tamponade from scarring and adhesions even without a pericardium
lung patient have pleural adhesions, complication chest tube placement
questions included in comprehensive travel history
dates of travel
what countries/how long in each
activities/where they stayed
tourist, adventure traveler or worker
cities vs. rural villages
sleeping in hotels or tents
sex?
eat/drink?
activities, ie. swimming in fresh water (schistosomiasis)
prophylactic immunizations prior to leaving?
malaria chemoprophylaxis and compliance?
mosquito repellent/netting use?
underlying chronic medical problems, medications
chronology of symptoms, particularly fever and diarrhea
what are the species responsible for causing human malaria
Plasmodium falciparum, Plasmodium vivax, Plasmodiumovale, Plasmodium malariae, Plasmodium knowlesi
clinical manifestations of malaria
cyclic or irregular fevers
anemia, h/a, nausea, chills, lethargy, abdo pain, upper resp complaints
what is the difference between P. falciparum aand other malari
falciparum causes severe organ system damage and death due to infected RBCs making sludge in arterioles and capillaries causing ischemia - manifested by cerebral malaria with cerebral deem and encephalopathy, hypoglycaemia, metabolic acidosis, severe anemia which may cause high output cardiac failure, renal failure, pulmonary edema, DIC
what is the gold standard for diagnosis of malaria
light microscopic examination of thick and thin blood films
treatment of malaria
in chloroquine-resistant regions: doxycycline or clindamycin, proguanil-atovaquone
for complicated falciparum infection: IV quinine or quinidine used
side effects of rapid infusion of quinine
profound hypoglycaemia, hyponatremia and coma vigil (neuroimpairment due to high rates of parasite destruction)
malaria treatment to prevent recrudescent disease in ovale, vivax
primaquine
who is primaquine contraindicated in
G6PD deficiency
what are the clinical manifestations of babesiosis
fatigue, anorexia, malaise, emotional lability, with myalgia, chills, high spiking fevers, sweats, h/a and dark urine
HSM, anemia, thrombocytopenia, leukopenia, elevated liver enzymes /hemolysis
what organism causes babesiosis
Babesia microti, gibsoni, and divergens
malaria-like illness due to protozoan similar in structure and life cycle to plasmodia
what areas of travel are at risk for babesiosis
NE US, NW US, Europe
endemic to Long Island, Cape Cod, Block Island
how to diagnosis babesiosis
multiple thick and thin smears
treatment of babesiosis
atovaquone plus azithromycin or for severe illness quinine plus clindamycin
how is babesiosis transmitted
deer tick Ixodes dammini
parasitic illnesses that cause significant fever
malaria babesiosis schistosomiasis leishmaniasis toxoplasmosis amebic liver abscess African and American trypanosomiasis fascioliasis
what is katayama fever
initial phase of schistosomiasis
spiking fevers, diaphoresis, wheezing and cough - eosinophilia common
exposure to fresh water in endemic areas
what is fascioliasis
liver fluke Fasciola hepatica - sheep/cattle exposure- metacercariae ingested in watercress
within 6 weeks, its get RUQ pain, fever, eosinophilia
what is American trypanosomiasis (Chagas disease)
endemic to Central/South America
reduviid bug sheds trypomastigotes proximal to bite site, host scratches skin - disease begins with chagoma at site often periorbital - progresses to fever, facial swelling, and pedal deem- parasitization of cardiac muscle leads to dysrhythmias and ventricular dysfunction
what is leishmaniasis
spread by sandflies and found in Middle East, India, East Africa, Brazil and along Mediterranean coast - can involve skin / mucosa, fever only seen with visceral involvement in immunocompetent persons
massive HSM, neutropenia, wt loss
how does Entamoeba histolytic present
amebic liver abscess
high fevers, RUQ pain, elevated WBC count
what parasitic infections are neurotrophic and cause neurologic symptoms
malaria
cysticercosis
echinococcosis
trypanosomiasis
examples of anthelmintic drugs
thiabendazole
mebendazole
albendazole
ivermectin
examples of trematodicide drugs
praziquantel use for flukes/schistosomes
example of antiprotozoal drugs
metronidazole
tinidazole
niridazole
example of antimalarial drug
chloroquine
mefloquine
proguanil-atovaquone
doxycycline
what bug causes cysticercosis and where do you get it
Taenia sodium - tropical areas - undercooked pork contains larval cysts
parasitemias that present with anemia
malaria
whipworm and hookworm
tapeworm
parasxitemias that present with peripheral edema
filarial infection or parasite-induced malnutrition and hypoproteinemia
elephantiasis or filariasis - Wuchereria bancrofti or Brugia malayi
parasites that present with derm symptoms
cutaneous leishmaniasis
dracunculiasis
cutaneous larva migrant (Anclyobranziliense larva) from dog/cat hookworm
swimmer’s itch - schistosome of avians/mammals
Strongyloides can cause transient pruritic rash
Taenia sodium cysts in soft tissue/muscle
onchocerciasis severe prurutius and nodules over bony proturuberances
parasites that present with visual symtpoms
onchocerciasis - major cause of blindness - microfiliaria migrates to eye , foreign tissue deposited in iris musculature incites immune sclerosis keratitis
loiasis - both in Africa
toxocariasis
toxoplasma gondii
parasites that present with pulmonary symptoms
P. falciparum E. histolytica Pneumocystis penumonia Strongyloides W. bancrofti, B.malayi E. granulosus - pulmonary hydatid cyst disease
parasites with CV symptoms
Chagas’ disease- Trypanosoma cruzi - in reduviid bug - usually bites near eye and forms chagoma - can lead to CHF
parasites that cause diarrha
Cryptosporidium pavum Cyclospora cayetanensis Entamoeba histolytica Balantidium coli Giardia lamblia S. stercoralis Capillaria philipinensis T. trichura Schistosome
which micro-organisms cause infective endocarditis
Staph aureus Viridans group streptococci Enterococci Coagulase-negative staphylococci Streptococcus bovid other streptococci non-HACEK, gram negative bacteria fungi HACEK polymicrobial culture negative other organisms
what are HACEK organisms
Haemophilus spp. Aggregatibacter actinomycetemcomitans Cardiobacterium hominis Eikenella corrodes Kingella kingae
symptoms associated with infective endocarditis
intermittent fever
malaise
weakness myalgia back pain dyspnea CP cough headaches anorexia
“classic” triad: fever, anemia, heart murmur
what diagnosis to think about stroke like symptoms and fever
endocarditis with septic emboli causing stroke like symptoms
physical exam findings in endocarditis
murmur
vasculitic lesions: petechia, splinter hemorrhages, Osler’s nodes, Janeway lesions
splenomegaly (30%)
ocular: conjunctival/retinal hemorrhages (pale center/surrounding red halo- Roth’s spot)
what are the major clinical criteria in Duke criteria
positive blood cultures (of typical pathogens) from at least 2 seperate cultures
evidence of endocardial involvement by echo: endocardial vegetation, paravalvular abscess, new partial dehiscence of prosthetic valve, new valvular regurgitation
what are the minor clinical criteria in Duke criteria
predisposition: heart condition or IVDU
fever: T > 38.0C
vascular phenomena: arteiral emobli, septic pulmonary infarcts, mycotic aneurysm, conjunctival hemorrhages or Janeway lesions
immunologic phenomena: Osler’s nodes, Roth’s spots and rheumatoid factor
microbio: single positive blood culture (except coag neg staph or organism that does NOT cause endocarditis)
echo findings: consistent with endocarditis but does not meet major criteria
how does duke criteria classify definite endocarditsi
2 major
1 major + 3 minor
5 minor
how does duke criteria classify possible endocarditis
1 major and 1-2 minor
3 minor
how does duke criteria classify rejected endocarditis
firm alternate diagnosis made
resolution of clinical manifestations occurs after 4 days or less of abx.
clinical criteria for possible or definite endocarditis not met
empiric abx for endocarditis in the ED
ceftriaxone 2g + 15mg/kg vancomycin
which endocarditis patients are appropriate for outpatient mgmt
HD stable, compliant, and capable of managing technical aspects of IV therpay
conditions requiring surgical therapy for infective endocarditis
infective endocarditis with acute heart failure fungal endocarditis periannular extension of infection recurrent emboli large mobile vegetations persistent bacteremia
which conditions are high risk for bacterial endocarditis and should have prophylaxis prior to certain procedures
prosthetic heart valve
hx. of endocarditis
unrepaired cyanotic CHD, including palliative shunts and conduits
completely repaired CHD with prosthetics during first 6 months after procedure
repaired CHD with residual defect at or adjacent to site of prosthetic
cardiac valvulopathy in a transplanted heart
jones criteria for diagnosis of acute rheumatic fever
major: carditis, polyarthritis, chorea, erythema marginatum, subcutaneous nodules
(JONES, joints, <3, nodules, erythema marginatum, sydenham’s chorea)
minor: arthralgia, fever, increased ESR/CRP, prolonged PR interval
evidence of preceding strep infection:
positive throat culture for group A beta-hemolytic strep or positive rapid antigen test
elevated or rising strep antibody tiger, usually anti-streptolysin O
what valve is most commonly affected in rheumatic fever
mitral - causing MR
treatment of acute rheumatic fever
penicillin 250mg kids or 500mg adults B-TID x 10 days
asa for arthritis
when should you culture an asbcess
complicated purulent infections, like surgical wound infections and abscesses in immunocompromised patientss
when to get blood cultures in skin infections
deep tissue infection or systemic infection likely ie. septic shock, necrotizing infections, immunocompromised, multifocal infections suggesting ghemoatogenous seeding and infections complicating lymphedema
likely bacterial cause and 1st line therapy for uncomplicated cutaneous abscess
CA-MRSA, others
I/D without abx.
likely bacterial cause and 1st line therapy for non purulent bacterial skin infections
various strep, staph aureus
keflex or clindamycin
likely bacterial cause and 1st line therapy for purulent cellulitis and wound infections
CA-MRSA, others
keflex + septra or clinda monotherpay
likely bacterial cause and 1st line therapy for diabetic foot infection
mixed gram-positive, gram negative and anaerobes
amox-clav + septra - avoid abx for uninfected ulcers
likely bacterial cause and 1st line therapy for any cat bite or infected dog bite
Pasteurella multiocida, others
amox-clav
likely bacterial cause and 1st line therapy for human bite
oral anaerobes, orhters
amox-clav
likely bacterial cause and 1st line therapy for erythema migrans
Borrelia burgdoferi (lyme) doxycycline
likely bacterial cause and 1st line therapy for puncture wound through sole of shoe
Pseudomonas aeruginosa
cipro
likely bacterial cause and 1st line therapy for buccal cellulitis
H. flu type b
ceftriaxone or amp-sulbactam
likely bacterial cause and 1st line therapy for balanitis
Candidia albicans or group A strep
fluconazole plus pen/amox; consider diabetes
likely bacterial cause and 1st line therapy for skin infection after liposuction
Peptostreptococcus (anaerobe), group A strep
amp-clav +/- septra
likely bacterial cause and 1st line therapy after skin infection with saltwater exposure
Vibrio vulnificus
doxycycline
likely bacterial cause and 1st line therapy for skin infection after freshwater exposure
Aeromonas species
cipro
likely bacterial cause and 1st line therapy for skin infection if pt is butcher, clam handler or veterinarian
Erysipelothrix rhusiopathiae
amoxicillin
likely bacterial cause and 1st line therapy for skin infection with black necrotic eschar with raised border and severe surrounding edema
Bacillus anthracis (anthrax) cipro
risk factor for Vibrio vulnificus infection
patients with liver disease/ cirrhosis
what is inducible resistance and when does it occur
CA-MRSA can be become resistant to clindamycin in single course of torment - about 2%
abx effective against MRSA
vancomycin septra clindamycin doxycycline linezolid daptomycin tigecycline telavancin
adjunctive measure to treat cellulitis
compression, elevation of extremity
NSAIDs
when do abscesses need abx after I/D
severe or extensive disease, severe associated cellulitis, signs and symptoms of systemic illness, associated comorbidities or immunosuppression, extremes of age,, abscess in an area difficult to drain, septic phlebitis, poor response to I/D
cause of impetigo
most S.aureus
some strep pyogenes
tx impetigo
nonbullous -topical mupirocin
extensive dz. or bullous- clinda or keflex+septra
mgmt of Bartholin cyst abscess
I/D, place Word catheter, test for GC/chlaydia
tx hot tub folliculutis
antihistamines, cipro
what causes hot tub folliculitis
Pseudomonas
treatment of folliculitis
hot compresses, mupirocin
AIDS-associated folliclutls - fungal or eosinophilic
isotretinoin topical or systemic antifungal
tx of fungal folliculitis
topical anitfungal
what is the distribution of hidradenitis supparativa
apocrine gland bearing skin - perineum, breasts, inner thighs, axilla
clinical manifestations of skin infection associated with necrotizing infection
signs of systemic toxicity, abnormal vitals, severe pain or pain out of proportion to physical exam findings, altered mental status, rapidly advancing infection, crepitus, hemorrhage sloughing and blistering
risk factors /inciting events for necrotizing skin/soft tissue infections
diabetes, vascular insufficiency, immunosuppression
inciting events: pentrating trauma, recent surgery, varicella infection, injection drug use, burns and childbirth
what are the two types of necrotizing fasciitis
Type I - polymicrobial with aerobes and anaerobes
Type II- single organism, usually GAS
tretment of suspected nec fasc
clindamycin, piptazo, Vanco
refer to surg ASAP
how to differentiate staphylococcal scalded skin syndrome from staphylococcal toxic shock syndrome
mucosa spared in SSSS,
components in MEDS (mortality in ED sepsis) score
terminal illness (death within 30 days) tachypnea/hypoxia septic shock platelet < 150 bands >5% age > 65 pneumonia NH resident AMS
DDX for sepsis
dehydration ARDS anemia ischemia hypoxia CHF vasculitis tox: poisoing, overdose, drug-induced pancreatitis hypothalamic injury DIC anaphylaxis metabolic hyperthyroidism DKA adrenal dysfunction: environment, burn, heat exhaustion/stroke trauma: blood loss, cardiac contusion NMS
hows does lactate correlate with mortality in sepsis
0-2.5 - 5% mortality
2.5-4 - 9% mortality
> 4 - 28% mortality
blood cultures in endocarditis ?
3 from 3 separate sites, 1 hour apart if possible
pt doesn’t have to be febrile, always bactermeic in IE
recommendedventilation in ARDS
plateau pressures below 35
TV 6ml/kg
dose of dobutamine infusion
5-15ug/kg/min
dose of dopamine infusion
2-20ug/kg/min
dose of epinephrine as vasopressor infusion
5-20ug/kg/min
dose of NE as infusion
5-20ug/kg/min
dose of phenylephrine infusion
2-20ug/kg/min
how does NE work
mixed alpha and beta agonist, minimal B2 activity
increases CO and SVR
how does dopamine work
precursor of epi and NE, acts on alpha, B1 and dopamine
side effects: persistent tachycardia, decreased PaO2, increased PA occlusion pressure
how does phenylephrine work
pure alpha1 agonist, increases SVR
can cause reflex bradycardia/suppress CO
may be useful when significant tachycardia limits use of another agent
how does epi work
mixed alpha and beta agonist
also associated with increased O2 consumption, increased splanchnic lactate concentrations, decreased splanchnic blood flow
how does vasopressin work
naturally occurring peptide in hypothalamus - initially early surge followed by profound drop in sepsis, which is the though behind using it
how does dobutamine work
mixed alpha and beta agonist, cardiac index is increased at expense of HR, decreased splanchnic blood flow
use in pt with depressed cardiac index and persistent hypo perfusion
initial abx management in patient with sepsis unknown source - immunocompetent
ceftazidime + aminoglycoside or fluroquinolone
piptazo + aminogylcoside or fluoroquinolone
carbapenem + amino glycoside or fluoroquinolone
initial abx management in patient with sepsis unknown source - suspected anaerobic infection
add metronidazole or clindamycin to piptazo + aminogylcoside or fluoroquinolone
initial abx management in patient with sepsis unknown source - MRSA
add vancomycin to piptazo + aminogylcoside or fluoroquinolone
initial abx management in patient with sepsis unknown source - splenectomy
ceftriaxone
initial abx management in patient with sepsis unknown source - HIV infection
ticarcillin-clavulanature + tobramycin
initial abx management in patient with sepsis - source pneumonia - immunocompetent
ceftriaxone + azithro or levo
initial abx management in patient with sepsis- source pneumonia - Legionella suspected
azithromycin or fluoroquinolone
initial abx management in patient with sepsis- source abdominal infection - immunocompetent
ampicillin + amino glycoside + metronidazole
initial abx management in patient with sepsis- source -MDRO suspected
ticarcilin-clavulanate or carbapenem or piptazo+aminoglyocside
initial abx management in patient with sepsis- source abdominal infection - urinary tract source
fluoroquinolone or ceftriaxone or ampicillin + aminogylcoside
initial abx management in patient with sepsis- source nonnecrotizing fasciits
cefazolin or nafcillin
initial abx management in patient with sepsis- source skin MRSA possible
vancomycin
initial abx management in patient with sepsis- source necrotizing fasciitis
piptazo + aminoglycoside + clinda
or ticarcillin-clav
or carbapenem
initial abx management in patient with sepsis- source IV catheter infection (remove cath) - outpatient acquired
ceftriaxone
initial abx management in patient with sepsis- source IV catheter infection (remove cath) - MRSA suspected
ceftriaxone + vancomycin
initial abx management in patient with sepsis- source IV catheter infection (remove cath) - fungal infection
amphotericin B
initial abx management in patient with sepsis- source CSF - immunocompetent
ceftriaxone + vanco
initial abx management in patient with sepsis- source CSF - older adult or immunocompromised
ceftriaxone + vancomycin + ampicillin
initial abx management in patient with sepsis- IVDU - MRSA not suspected
nafcillin + aminoglycoside
initial abx management in patient with sepsis- IVDU - MRSA suspected
vancomycin +aminoglycoside
antibiotics that cover pseudomonas
- Antipseudomonal cephalosporin (eg, ceftazidime, cefepime), or
- Antipseudomonal carbapenem (eg, imipenem, meropenem), or
- Antipseudomonal beta-lactam/beta-lactamase inhibitor (eg, piperacillin-tazobactam, ticarcillin-clavulanate), or
- Fluoroquinolone with good anti-pseudomonal activity (eg, ciprofloxacin)
- Aminoglycoside (eg, gentamicin, amikacin), or
- Monobactam (eg, aztreonam)
what are the serious bacterial infections in paediatric fever referring to
UTI, bacteremia, meningitis, osteomyelitis, bacterial gastro, bacterial pneumonia, cellulitis, and septic arthritis
causes of fever in 0-28 day old
bacterial: GBS, E.coli, Listeria, Chlamydia trachomatis, Neissseira gonorrhea, Strep pneumo
viral: HSV, varicella, enteroviruses, RSV, influenza
other: bundling, environmental
cause of fever in 1-3 month old
bacterial: H. flu, Strep pneumo, Neisseria meningitis, E.coli
viral: varicella, enteroviruses, RSV, influenza
other: environmental
cause of fever in 3-36months
bacterial: Strep pneumo, N. meningitidis, E.coli
viral: varicella, enteroviruses,RSV, influenza, mononucleosis, roseola, adenovirus, norwalk virus, coxsackievirus
other: leukemia, lymphoma, neuroblastoma, wilms tumor
cause of fever in 3 years to adulthood
bacterial: Strep pneumo, N. meningitidis, E.coli, GAS
viral: varicella, enteroviruses, RSV, influenza, mononucleosis, roseola, adenovirus, norwalk virus
other: leukemia, lymphoma, neuroblastoma, Wilms’ tumor, juvenile rheumatoid arthritis
what workup is needed after UTI is diagnosed in infant
ultrasound to look for hydronephrosis or renal/perirenal abscesses
VCUG only needed if abnormal US
what peds groups are high risk for UTI
febrile girls under 24 months
uncircumcised boys under 12 months
circumcised boys under 6 months
contraindications for lumbar puncture in peds
cellulitis over proposed site of puncture, CP instability, bleeding diathesis, or platelet count below 50, focal neuro deficits, signs of increased ICP including papilledema
how to differentiate children with bacterial vs. aseptic meningitis
kids without any of hte following have less than 0.1% risk of bacterial meningitis: positive CSF gram stain, CSF ANC of 1000 cells/ml or more, CSF protein of at least 80mg/dL, peripheral blood ANC of 10,000 mL or more, and history of seizure before or at time of presentation
when to get CXR in febrile child
hypoxemia, resp distress, tachypnea, or focal findings on lung exam
in high febrile kids with no source of infection - occult pnuemonia risk 9% - get CXR
RSV with other SBI - what workup needed
in kids UTI risk 7% still with RSV positive - so get urine/culture
amount of fluids to give kid with signs of shock (poor perfusion, hypotension, altered)
20cc/kg bolus of crystalloid, repeat up to 60cc/kg in 60 mins then think about pressors
when to consider neonatal HSV
febrile neonate with maternal hx of genital herpes, or who appears ill with fever/seizure, has cutaneous vesicles on physical exam or evidence of transminitis or coagulopathy
non infectious causes of septic appearing neonate
acute salt wasting crisis in CAH, undiagnosed ductal dependent CHD
workup required for infant 0-28 days with fever
CBC, blood cultures, UA + culture, and lumbar puncture
CXR, stool prn
treatment of neonate 0-28 days with fever
ampicillin (100mg/kg/day in q6h doses) plus gentamicin (5mg/kg/day in q8-12h doses) or ampicillin plus cefotaxime (150mg/kg/day in q8h doses)
add acyclovir (60mg/kg/day in q8h doses) if any one of following: ill-appearing, skin or mucosal lesions consistent with HSV, CSF pleocytosis, seizure, focal neuro sign, abnormal neuroimaging, respiratory distress, apnea or progressive pneumonitis, thrombocytopenia, elevated transaminases viral hpeattis or acute lvier fialure, coonjunctivitis, excessive tearing, orpainful eye symptoms
treatment of infant 29-90 days old with fever
ampicillin 50-100mg/kg q6h plus cefotaxime 50mg/kg q8h
add vanco 10-20mg/kg IV q6-8h if concerned about Strep pneumonia resistant to pen/cephalosporins
what is Rochester criteria
history: term infant, no perinatal abx, no underlying disease, not hospitalized longer than mother
physical: well-appearing, no ear/soft tissue/bone infection
labs: WBC 5-15, absolute bands < 1.5, urine <10 WBC/hpf, stool <5 WBC/hpf
what workup needed according to Rochester criteria
minimum: CBC, cath UA and urine culture, then
blood culture if WBC abnormal
CXR if respiratory symptoms
LP if WBC abnormal
what are the disposition options for infant 29-90 days old with fever
low risk infant- must have reliable caregiver
- option 1: no abx and close f/u in 24 hours
- option 2: ceftriaxone IV/IM after LP with close f/u in 24 hours
high risk infant: admit to hospital for ceftriaxone IV/IM
what workup needed for Boston criteria
CBC, blood culture, LP, urine + culture, +/- CXR, ABX prior to D/C
what workup needed for Philadelphia critera
CBC, blood culture, urine+ culture, LP, CXR, no ABX prior o DC`
what work up needed for kids3 month - 3 years with fever
fever defined as above 39 in this age group
clinical judgment - toxic vs. nontoxic
nontoxic kids-
CBC, blood culture
urine /culture for girls under 24 mo, circumcised boys under6 mo, uncircumcised boys under 12 mo
+/- CXR, stool
abx if WBC above 15k
what is rate of epilepsy after febrile seizure
gen pop epilepsy - 0.5-1%
after febrile seizure - 1-2%
what is rate of recurrence after febrile seizure
33% will have another one, 75% of which in one year of time
if kid is under age 1, and temp of 38.5C - 35% chance of recurrent vs. 13% if temp 40C
what classifies a simple febrile seizure
brief < 15 mins
non focal
single occurrenceli
what kids need LP after febrile seizure
workup for source of fever
kid with signs of meningeal irritation after first febrile seizure
symptomatic kids that are incompletely immunized or have recevied prior abx therapy
differential diagnosis for fever + petechiae
meningococcemia RMSF DIC pneumococcal bacteremia Strep pyogenes infection viral infections ITP HSP leukemia
petechiae can be caused by vomitting or cough but are typically confined above the nipple line vs. SBI petechiae have any distribution
what tests to order for kid with fever + petechiae
CBC, CRP, blood cultures -if abnormal admit and treat until blood cultures negative
if normal blood work and well appearing cacn send home without abx as long as close outpatient followup
what abx are used in sickle cell kids
penicillin 125mg PO BID until 3 years old, then 250g BID until age 5 - can be DC in kids if not prior severe pneumococal infection or surgical splenectomy
what bug often causes infection in Sickle cell kids
Salmonella - osteomyelitis, gastroenteritis
what workup needed for Sickel cell kids with fever
CBC, reticulocyte count, ESR, blood culture,
acute HIV infection clinical manifestatiosn
fever, pharyngitis, LAD 2-6 weeks after transmission
neuro: cases of GBS, encephalitis, and mono neuritis have occurred
AIDS defining conditions
bacterial infections - multiple or recurrent
candidiasis of broncho, trachea, lungs, or esophagus
cervical cancer- invasive
coccidioidomycosis - disseminated or extrapulmonary
cryptococcus, extra pulmonary
cryptosporidiosis, chronic intestinal (>1mo duration)
CMV disease (other than liver, spleen or nodes), onset at age >1mo
CMV retinitis (w loss of vision)
HIV encephalopathy
HSV - chronic ulcers (>1 mo duration) or bronchitis, pneumonitis, or esophagitis (onset at age >1mo)
histoplasmosis - disseminated or extrapulmonary
isosporiasis, chronic intestinal > 1mo duration
Burkitt’s lymphoma
Kaposi’s sarcoma
immunoblastic lymphoma
CNS lymphoma
MAC or mycobacterium kansasii, disseminated or extra pulmonary
TB
other mycobacterium
PCP
pneumonia, recurrent
progressive multifocal leukoencephalopathy
Salmonella septicemia
toxoplasmosis of brain
wasting syndrome attributed to HIV
what abx prophylaxis regimens are usedin HIV
Pneumocystis jiroveci pneumonia (PCP) prophylaxis when CD4 < 200 with septra
toxoplasma gondii encephalitis prophylaxis if CD4 < 100, and IgG positive - with septra
MAC prophylaxis when CD4 under 50 with azithromycin
common clinical presenation of Toxoplasma encephalitis in HIV pt
fever, h/a, AMS, focal neuro findings, seizure, evolves during days to weeks
imaging/diagnostic test findings in Toxoplasma encephalitis in HIV
ring enhancing CNS lesions frequent edema nd mass effect toxoplasma antibodies (reflects past exposure) CD4 often <100cells/uL PCR detection of Toxoplasma gondii
common clinical presentation of primary CNS lymphoma (PCNSL) in HIV pt
confusion, lethargy, memory loss, hemiparesis, aphasia, seizure, fever, night sweats, weight loss, evolves during months
imaging/diagnostic test findings in primary CNS lymphoma
CNS lesion or lesions (may have mass effect)
solitary lesions are often large (>4cm)
some ring enhancement may occur but less regular
PCR assay for EBV associated with PCNSL
common clinical presentation of progressive multifocal leukoencephalopathy
progressive focal neuro deficits (during months), hemiparesis, visual field defects, ataxia, aphasia, cognitive impairment
imaging/diagnostic test findings in PML
multifocal areas of demyelination primarily involving white matter
less frequent mass effect or ring-enhancing
PCR assay for DNA of JC virus
common clinical presentation of HIV encephalopathy
memory and psychomotor speed impairment, depressive symptoms, movement disorders
imaging/diagnostic test findings in HIV encephalopathy
multiple hyperintesine signals in T2-weighted images
often symmetric, not well demarcated
common clinical presentation in CMV encephalitis
delirium, confusion, focal neuro abnormalities
imaging/diagnostic tests in CMV encephalitis
MRI shows multifocal scattered micro nodules and ventriculoencephalitis
CD4 < 50 cells/uL
common clinical presentation of brain abscess
focal neuro deficit, h/a, bacteremia or craniofacial infection
imaging and diagnostic tests in brain abscess
often concomitant evidence of disseminated infection
focal ring-enhancing lesion
common clinical manifestation of tuberculoma
focal neuro deficit, h/a, tuberculous infection
imaging/diagnostic tests in tuberculoma
single or multiple mass lesions
can be manifested as focal lesion or meningeal infection
dermatologic and mucocutaneous manifestations of WHO Stage 4 HIV disease
chronic HSV ulcers extrapulmonary tuberculosis Kaposi's sarcoma extrapulmonary cryptococcosis disseminated mycosis atypical disseminated leishmaniasis disseminated nontuberculous mycobacterial infection extra pulmonary cryptococcosis including meningitis
what renal manifestations of HIV occur
HIVAN -HIV associated nephropathy - FSGS
vs. HIV immune complex kidney disease
DDX of respiratory infections in HIV patients by CD4 counts
any CD4- acute bronchitis, bacterial pneumonia, tb
> 500 CD4 - bacterial pneumonia
early HIV infection- PCP, HHV-8 related Kaposi’s sarcoma
200-500- bacterila pneumonia, PCP
< 200, bacterial pneumonia
AIDS - PCP, histoplasma capsulation or Coccidiodes immitis pneumonia, Cryptococcus neoformans pneumonia, extra pulmonary or disseminated tb
<50 CD4- bacterial pneumonia
advanced HIV infection - PCP, toxoplasma gondii pneumonia, pulmonary Kaposi’s sarcoma, histoplasma / Coccidiodes, MAC
clinical manifestations/diagnostic labs of bacterial pneumonia in HIV
acute onset, <1 week, cough, purulent sputum ,fevers, chills, rigors
elevated WBC, CXR- focal consolidation, CD4 variable
treatment of bacterial pneumonia in HIV
abx against Strep pneumo and H. flu, also cover atypical pathogens
ie. ceftriaxone, azitho.
clinical manifestations/diagnostic labs in PCP
gradual onset > 2 week, non productive cough, dyspnea, fever
exercise-induced hypoxia, elevated LDH, CXR- bilateral reticular or interstitial pattern, CT -ground glass opacity 56%, CD4 < 200
treatment of PCP
septra x 21 days, if PaO2 < 70 on r/a, or A-a gradient > 35, give prednisone, taper over 21 days
clinical manifestations/diagnostic labs in TB in HIV pt
gradual onset > 2 weeks, cough, fever, night sweats, weight loss, LAD
CXR- alveolar pattern +/- cavitation, military pattern, nodules, adenopathy, effusions
CD4 variable
clinical manifestations/diagnostic labs of Kaposi’s sarcoma
gradual onset >2-4 weeks, cough, dyspnea, fever
CXR- bilateral perihilar nodules, opacities, effusions, adenopathy
CD4 <200
treatment of Kaposi’s sarcoma
cryotherapy, radiation therapy
infrared coagulation
sclerosing agents, intralesional vinblastine
systemic chemo
treatment of esophageal candidiasis
fluconazole po - should have clinical response in 5-7 days
if no response - endoscopy for biopsy as ddx includes candidiasis, HSV, CMV, deep apthous ulcers
cutaneous findings highly suggestive of HIV disease
any WHO criteria for stage 4 disease facial molluscum in an adult proximal subungal onychomycosis herpes zoster scarring oral hairy leukoplakia bacillary angiomatosis widespread dermatophytosis severe seborrheic dermatitis