Emergency Medicine EOR (2026): Infectious Diseases (Smarty PANCE)

What is bacteremia?

The presence of viable bacteria in the bloodstream, which may be transient and benign or the driver of sepsis, metastatic infection, and endocarditis.

How should blood cultures be obtained in the ED to maximize yield and interpretability?

Two sets (aerobic and anaerobic) from two separate venipuncture sites, drawn before antibiotics, with adequate volume (10 mL per bottle in adults) since volume is the single biggest determinant of yield.

Which findings suggest a blood culture is a contaminant rather than true bacteremia?

Growth in only one of two sets, prolonged time to positivity (greater than 48 hours), and typical skin flora such as coagulase-negative staphylococci, Corynebacterium, Bacillus, or Cutibacterium acnes.

Why is Staphylococcus aureus in a blood culture never treated as a contaminant?

S. aureus bacteremia carries high rates of endovascular seeding and metastatic infection, so it always requires IV antibiotics, source control, repeat cultures to document clearance, and echocardiography to evaluate for endocarditis.

What is the most common source of health care-associated bacteremia presenting to the ED?

Indwelling intravascular catheters, followed by urinary catheters and surgical or wound sites; catheter removal is often required for source control.

Which patients are at risk for fulminant bacteremia from encapsulated organisms?

Asplenic or functionally asplenic patients (including sickle cell disease), who can rapidly decompensate from Streptococcus pneumoniae, Haemophilus influenzae, or Neisseria meningitidis and need immediate empiric antibiotics.

What ED findings should prompt evaluation for infective endocarditis in a bacteremic patient?

Persistent bacteremia despite therapy, injection drug use, prosthetic valve or intracardiac device, new murmur, or embolic phenomena such as septic pulmonary emboli, Janeway lesions, or Osler nodes.

What is tetanus?

A neuroparalytic disease caused by the exotoxin tetanospasmin from Clostridium tetani, producing unopposed muscle rigidity and spasm after spores contaminate a wound.

What is the mechanism of tetanospasmin?

It blocks presynaptic release of the inhibitory neurotransmitters glycine and GABA from Renshaw cells in the spinal cord, causing loss of inhibition and sustained muscle contraction.

What are the classic clinical features of generalized tetanus?

Trismus (lockjaw) as the earliest sign, risus sardonicus, opisthotonus, board-like abdominal rigidity, and painful spasms with a fully intact sensorium.

What autonomic complication drives mortality in severe tetanus?

Autonomic instability with labile hypertension alternating with hypotension, tachyarrhythmias, and diaphoresis, typically peaking in the second week and requiring magnesium sulfate and short-acting agents such as esmolol.

How is tetanus diagnosed in the ED?

Clinically — it is a bedside diagnosis based on the history and exam, since cultures are positive in fewer than one third of cases and there is no confirmatory test.

What is the ED management of active tetanus?

Human tetanus immune globulin (HTIG) to neutralize unbound toxin, wound debridement, metronidazole as the preferred antibiotic, benzodiazepines for spasms, tetanus toxoid vaccine at a separate site, and a quiet dark room to minimize stimulation.

What are the tetanus prophylaxis rules for wound care?

Clean minor wound: Td/Tdap if the last dose was more than 10 years ago. Dirty or high-risk wound: Td/Tdap if more than 5 years ago, plus tetanus immune globulin if the patient has fewer than 3 lifetime doses or unknown vaccination status.

What is necrotizing fasciitis?

A rapidly progressive, limb- and life-threatening infection that spreads along the fascial planes causing tissue necrosis, systemic toxicity, and high mortality without emergent surgical debridement.

What is the hallmark early clinical clue to necrotizing fasciitis?

Pain out of proportion to the physical exam findings, often with an unremarkable-appearing overlying skin in the earliest hours.

What are the late "hard signs" of necrotizing fasciitis?

Crepitus, hemorrhagic bullae, skin anesthesia, dusky or necrotic skin, and rapid progression of erythema margins — their absence does not rule out the disease.

How do Type I and Type II necrotizing fasciitis differ?

Type I is polymicrobial (aerobes plus anaerobes) in diabetics, the elderly, and postoperative patients. Type II is monomicrobial, most often group A Streptococcus pyogenes, and can strike healthy young patients.

What is the LRINEC score and its limitation?

A risk-stratification score using CRP, WBC, hemoglobin, sodium, creatinine, and glucose; it can support suspicion but a low score does not exclude necrotizing fasciitis and must never delay surgical consultation.

What imaging finding suggests necrotizing fasciitis and what is the caveat?

Soft tissue gas tracking along fascial planes on plain film or CT, but gas is present in a minority of cases and imaging should never delay operative exploration in an unstable patient.

What is the definitive treatment for necrotizing fasciitis?

Emergent surgical exploration and wide debridement — antibiotics and resuscitation are adjuncts, and time to the operating room is the strongest predictor of survival.

What empiric antibiotic regimen is used for necrotizing fasciitis?

Broad-spectrum coverage such as vancomycin or linezolid plus piperacillin-tazobactam or a carbapenem, PLUS clindamycin for its antitoxin effect through ribosomal suppression of streptococcal exotoxin production.

What is Fournier gangrene?

Necrotizing fasciitis of the perineal, genital, and perianal region, most often polymicrobial, seen in diabetics, alcoholics, and immunocompromised patients, requiring emergent urologic or surgical debridement.

What is pertussis?

A highly contagious respiratory infection caused by Bordetella pertussis producing a prolonged paroxysmal cough illness that is most dangerous in infants under 6 months.

What are the three clinical stages of pertussis?

Catarrhal (1-2 weeks of URI symptoms, most contagious), paroxysmal (2-6 weeks of coughing fits with inspiratory whoop and post-tussive emesis), and convalescent (weeks to months of gradually resolving cough).

How does pertussis present differently in young infants?

Infants often lack the classic whoop and instead present with apnea, cyanosis, bradycardia, poor feeding, or seizures — apnea may be the only manifestation and warrants admission and monitoring.

What laboratory finding is characteristic of pertussis?

A marked lymphocyte-predominant leukocytosis; extreme leukocytosis (greater than 50,000) in an infant predicts pulmonary hypertension and death.

What is the diagnostic test of choice for pertussis?

Nasopharyngeal PCR, which has the highest yield in the first 3-4 weeks of cough; culture is specific but slow and serology is useful only late in the illness.

What is the treatment for pertussis and what does it accomplish?

A macrolide (azithromycin preferred) — it reduces transmission and shortens the contagious period but does not shorten the cough once the paroxysmal stage has begun unless started early.

Which macrolide is preferred in infants under 1 month and why?

Azithromycin, because erythromycin in this age group is associated with infantile hypertrophic pyloric stenosis.

Who should receive post-exposure prophylaxis for pertussis?

All household and close contacts regardless of vaccination status, using the same macrolide regimen, with priority given to infants, pregnant women in the third trimester, and those in contact with infants.

What is encephalitis?

Inflammation of the brain parenchyma producing altered mental status, personality change, seizures, or focal neurologic deficits, most often from a viral infection.

How is encephalitis clinically distinguished from meningitis?

Meningitis causes fever, headache, and meningismus with a preserved sensorium, while encephalitis is defined by altered mental status, behavioral change, seizures, or focal deficits — the two frequently overlap as meningoencephalitis.

What is the most common cause of sporadic fatal encephalitis in the United States?

Herpes simplex virus type 1, which has a predilection for the temporal and inferior frontal lobes.

What CSF and imaging findings suggest HSV encephalitis?

CSF with lymphocytic pleocytosis, elevated protein, normal glucose, and often red blood cells or xanthochromia from hemorrhagic necrosis; MRI shows temporal lobe involvement and EEG may show periodic lateralized epileptiform discharges.

What is the most critical ED action when HSV encephalitis is suspected?

Start IV acyclovir 10 mg/kg every 8 hours immediately — do not wait for CSF PCR results, MRI, or lumbar puncture, since delay dramatically increases mortality and disability.

What is the diagnostic gold standard for HSV encephalitis?

CSF HSV PCR, which is highly sensitive and specific, though it can be falsely negative if obtained within the first 72 hours of symptoms and should be repeated if suspicion remains.

What autoimmune cause of encephalitis should be considered in a young patient with psychiatric symptoms and seizures?

Anti-NMDA receptor encephalitis, which presents with prominent psychiatric features, movement disorders, and autonomic instability, and in young women is associated with ovarian teratoma.

What is fever of unknown origin (FUO)?

A temperature of 38.3 degrees C (101 degrees F) or higher on several occasions, lasting more than 3 weeks, that remains undiagnosed after an appropriate initial evaluation.

What are the four classic diagnostic categories of FUO?

Infection, malignancy, autoimmune and connective tissue disease, and miscellaneous causes including drug fever, factitious fever, and thromboembolic disease.

What is the primary role of the emergency clinician in a patient with FUO?

To identify and treat the immediately life-threatening causes and determine disposition — not to complete the diagnostic workup, which is generally an inpatient or outpatient endeavor.

What are the most common infectious causes of FUO worldwide?

Tuberculosis (especially extrapulmonary and miliary), occult abscesses, and infective endocarditis with fastidious or culture-negative organisms.

Which patients with prolonged fever require immediate empiric antibiotics in the ED?

Those who are hemodynamically unstable, neutropenic (ANC less than 500), asplenic, or otherwise significantly immunocompromised — otherwise empiric antibiotics obscure the diagnosis.

What noninfectious cause of prolonged fever in patients over 50 requires urgent treatment to prevent blindness?

Giant cell arteritis — start high-dose corticosteroids immediately when suspected, before temporal artery biopsy.

What is fever without a source?

An acute febrile illness in a child with no identifiable cause after a thorough history and physical examination, where the key ED task is identifying occult serious bacterial infection.

What temperature defines fever in an infant and how should it be measured?

A rectal temperature of 38.0 degrees C (100.4 degrees F) or higher; rectal measurement is the standard in infants, and a reliable history of tactile or measured fever at home counts.

What is the ED approach to a febrile neonate 28 days old or younger?

Full evaluation including blood culture, urine culture by catheterization, and lumbar puncture, with admission and empiric parenteral antibiotics (typically ampicillin plus gentamicin or ampicillin plus ceftazidime).

When should acyclovir be added for a febrile neonate?

When there are HSV risk factors or findings such as maternal genital lesions, vesicles, seizures, CSF pleocytosis, elevated transaminases, or ill appearance — neonatal HSV can present without skin lesions.

What are the "big three" pathogens driving management of the febrile neonate?

Group B Streptococcus, Escherichia coli, and Listeria monocytogenes, with herpes simplex virus as the critical viral consideration.

What is the highest-yield single test in a well-appearing immunized febrile child aged 3 to 36 months?

Urinalysis with urine culture, since urinary tract infection is the most common occult serious bacterial infection in this group.

How did conjugate vaccines change the risk of occult bacteremia in febrile toddlers?

Widespread Haemophilus influenzae type b and pneumococcal conjugate vaccination has reduced occult bacteremia to well under 1 percent, so routine blood cultures and empiric antibiotics are no longer indicated in the well-appearing, fully immunized child.

What is the most important assessment in any febrile child regardless of age?

Overall appearance and perfusion — an ill-appearing or toxic child requires a full sepsis evaluation, empiric antibiotics, and admission no matter what the risk-stratification criteria suggest.

What are the emergency-relevant fungal infections?

Invasive or opportunistic infections caused by yeasts and molds, which most often threaten immunocompromised, diabetic, or critically ill patients and can be rapidly fatal without early antifungal therapy.

What is the classic ED presentation of cryptococcal meningitis?

A subacute headache with fever and altered mentation in an HIV patient with CD4 count under 100, often with minimal meningismus and markedly elevated CSF opening pressure.

How is cryptococcal meningitis diagnosed and initially treated?

Cryptococcal antigen in serum or CSF (India ink shows encapsulated yeast), treated with amphotericin B plus flucytosine for induction, along with serial lumbar punctures to control elevated intracranial pressure.

What is rhinocerebral mucormycosis and who gets it?

An angioinvasive mold infection in patients with diabetic ketoacidosis, hematologic malignancy, or deferoxamine use, presenting with facial pain, black necrotic eschar of the palate or turbinates, and cranial neuropathies.

What is the treatment of mucormycosis?

Emergent surgical debridement plus IV liposomal amphotericin B and correction of the underlying acidosis or immunosuppression — mortality is high and surgery cannot be delayed.

What is coccidioidomycosis and where is it endemic?

"Valley fever" caused by Coccidioides species, endemic to the San Joaquin Valley, the desert Southwest, and parts of Central and South America, presenting with pneumonia, erythema nodosum, and arthralgias (desert rheumatism).

Which fungal infection is an AIDS-defining illness when it involves the esophagus?

Esophageal candidiasis, which presents with odynophagia and dysphagia, often with visible oral thrush, and warrants systemic fluconazole rather than topical therapy.

What is the significance of candidemia found in the ED?

Candida in blood cultures is never a contaminant — it requires an echinocandin, removal of central venous catheters, and ophthalmologic examination for endophthalmitis.

What is toxoplasmosis?

An infection caused by the intracellular protozoan Toxoplasma gondii, acquired from cat feces or undercooked meat, that is usually asymptomatic but causes severe CNS disease in immunocompromised patients and congenital infection in the fetus.

What is the classic ED presentation of CNS toxoplasmosis?

Headache, fever, focal neurologic deficits, or seizures in a patient with advanced HIV and a CD4 count below 100.

What is the characteristic neuroimaging finding of cerebral toxoplasmosis?

Multiple ring-enhancing lesions with surrounding edema, classically in the basal ganglia and at the gray-white junction.

How is cerebral toxoplasmosis distinguished from primary CNS lymphoma?

Toxoplasmosis typically causes multiple lesions and responds to empiric therapy within 2 weeks; CNS lymphoma is more often a single periventricular lesion, is thallium SPECT avid, and is associated with EBV DNA in the CSF.

What is the treatment for CNS toxoplasmosis?

Pyrimethamine plus sulfadiazine plus leucovorin (folinic acid to prevent bone marrow suppression), with TMP-SMX as an alternative regimen.

What is the classic triad of congenital toxoplasmosis?

Chorioretinitis, hydrocephalus, and diffuse intracranial calcifications.

What is sepsis?

Life-threatening organ dysfunction caused by a dysregulated host response to infection, defined by an acute increase of 2 or more points in the SOFA score.

What defines septic shock under the Sepsis-3 definitions?

Sepsis with persistent hypotension requiring vasopressors to maintain a mean arterial pressure of 65 mmHg or greater AND a serum lactate greater than 2 mmol/L despite adequate volume resuscitation.

What are the qSOFA criteria and how should they be used?

Respiratory rate 22 or greater, altered mentation, and systolic blood pressure 100 mmHg or less — 2 or more suggests higher mortality risk, but qSOFA is a prognostic prompt, not a screening tool sensitive enough to rule out sepsis.

What are the components of the Surviving Sepsis Hour-1 bundle?

Measure lactate, obtain blood cultures before antibiotics, administer broad-spectrum antibiotics, begin 30 mL/kg crystalloid for hypotension or lactate 4 mmol/L or greater, and start vasopressors if hypotension persists during or after fluids.

What is the first-line vasopressor in septic shock?

Norepinephrine, with vasopressin added as a second agent to reduce norepinephrine requirement and epinephrine considered when a third agent is needed.

Why is elevated lactate important in sepsis even without hypotension?

Lactate 4 mmol/L or greater identifies cryptic shock with mortality comparable to overt hypotension, and failure to clear lactate on repeat measurement predicts poor outcome.

What is the most important determinant of survival in septic shock besides antibiotics?

Source control — draining an abscess, removing an infected catheter, or operating on necrotic or perforated tissue, ideally within 6 to 12 hours of recognition.

Which patients with sepsis should receive stress-dose corticosteroids?

Those with septic shock refractory to adequate fluid resuscitation and ongoing vasopressor requirement, typically hydrocortisone 200 mg per day.

What are sexually transmitted infections?

Infections transmitted through sexual contact that in the ED demand syndromic recognition, empiric therapy at the visit, partner management, and reporting, since follow-up is often unreliable.

What is the current CDC-recommended treatment for uncomplicated gonorrhea?

Ceftriaxone 500 mg IM as a single dose (1 g if the patient weighs 150 kg or more), with doxycycline 100 mg twice daily for 7 days added if chlamydia has not been excluded.

What is the treatment for uncomplicated chlamydial infection?

Doxycycline 100 mg twice daily for 7 days, which is now preferred over single-dose azithromycin; azithromycin 1 g once remains the option in pregnancy.

What are the minimum diagnostic criteria for pelvic inflammatory disease?

Cervical motion tenderness, uterine tenderness, or adnexal tenderness in a sexually active woman with pelvic pain and no other identified cause — treat empirically because the threshold for diagnosis is deliberately low.

What is the outpatient regimen for pelvic inflammatory disease?

Ceftriaxone 500 mg IM once plus doxycycline 100 mg twice daily for 14 days plus metronidazole 500 mg twice daily for 14 days.

What is the classic triad of disseminated gonococcal infection?

Migratory polyarthralgia, tenosynovitis, and a pustular or vesiculopustular dermatitis, which may progress to a purulent monoarticular septic arthritis.

How do the stages of syphilis present?

Primary — a single painless indurated chancre; secondary — diffuse maculopapular rash involving the palms and soles with condylomata lata and constitutional symptoms; tertiary — gummas, aortitis, and neurosyphilis.

What is the treatment for primary, secondary, or early latent syphilis?

Benzathine penicillin G 2.4 million units IM as a single dose; penicillin-allergic nonpregnant patients may receive doxycycline, but pregnant patients must be desensitized and treated with penicillin.

What is the Jarisch-Herxheimer reaction?

An acute febrile reaction with headache, myalgias, and rigors occurring within 24 hours of treating spirochetal infection, caused by release of endotoxin-like products from dying organisms — managed supportively, not as an allergy.

How are genital ulcer diseases differentiated?

Syphilis produces a single painless ulcer with a clean base and firm induration; chancroid (Haemophilus ducreyi) produces painful, deep, purulent ulcers with tender suppurative buboes; HSV produces multiple painful shallow vesicles and ulcers.

What is the ED presentation and treatment of trichomoniasis?

Frothy malodorous yellow-green discharge with a strawberry cervix and motile trichomonads on wet mount, treated with metronidazole (7-day course preferred in women) plus partner treatment.

What are vector-borne infections?

Diseases transmitted to humans by arthropod vectors such as ticks, mosquitoes, fleas, and lice, in which exposure history, geography, and season are as diagnostically important as the physical exam.

What is the classic rash of Rocky Mountain spotted fever?

A maculopapular rash beginning on the wrists and ankles around day 3 to 5, spreading centripetally to the trunk, and involving the palms and soles, later becoming petechial.

What is the treatment of Rocky Mountain spotted fever and the critical pitfall?

Doxycycline in all patients including children under 8 — start empirically on clinical suspicion, because waiting for confirmatory serology or withholding doxycycline in a child dramatically increases mortality.

What skin finding is pathognomonic for early Lyme disease and how is it managed?

Erythema migrans, an expanding annular lesion often with central clearing — treat clinically with doxycycline without serologic testing, since antibodies have usually not yet developed.

What are the cardiac and neurologic manifestations of early disseminated Lyme disease?

Lyme carditis with variable and often high-grade AV block, and neuroborreliosis with cranial neuropathy — classically a unilateral or bilateral facial nerve palsy — plus lymphocytic meningitis and radiculopathy.

What is babesiosis and who develops severe disease?

A malaria-like intraerythrocytic protozoal infection transmitted by Ixodes ticks causing fever and hemolytic anemia with the "Maltese cross" tetrad on smear; asplenic, elderly, and immunocompromised patients develop severe disease.

What laboratory triad suggests ehrlichiosis or anaplasmosis?

Leukopenia, thrombocytopenia, and elevated transaminases in a febrile patient with tick exposure; morulae may be visible in leukocytes, and treatment is doxycycline.

What features suggest severe malaria requiring IV artesunate?

Parasitemia greater than 5 percent, impaired consciousness or seizures, acidosis, hypoglycemia, renal failure, ARDS, or jaundice — almost always due to Plasmodium falciparum in a returning traveler.

Why should NSAIDs be avoided in suspected dengue fever?

Dengue causes thrombocytopenia and increased vascular permeability, so NSAIDs and aspirin increase bleeding risk; acetaminophen is the analgesic of choice.

What is tick paralysis and how is it treated?

An ascending flaccid paralysis with areflexia and preserved sensation caused by a neurotoxin from an attached engorged tick, mimicking Guillain-Barre syndrome, and cured by finding and removing the tick.

What is Clostridioides difficile infection?

A toxin-mediated colitis caused by overgrowth of C. difficile after disruption of normal gut flora, most often by antibiotics, ranging from mild diarrhea to fulminant colitis and toxic megacolon.

Which antibiotics most commonly precipitate C. difficile infection?

Clindamycin, fluoroquinolones, cephalosporins, and penicillins — though virtually any antibiotic can be implicated, and risk persists for up to 3 months after exposure.

How is C. difficile infection diagnosed?

Testing of unformed stool only, using a two-step algorithm of glutamate dehydrogenase antigen plus toxin EIA, or NAAT/PCR — never test formed stool or perform a test of cure, as colonization is common.

What is the current first-line treatment for an initial nonsevere episode of C. difficile?

Oral vancomycin 125 mg four times daily for 10 days or oral fidaxomicin; metronidazole is now reserved for when neither is available.

How is fulminant C. difficile colitis treated?

High-dose oral or nasogastric vancomycin 500 mg four times daily PLUS IV metronidazole, with rectal vancomycin retention enemas if ileus is present, and emergent surgical consultation for colectomy.