01Approach to the Critical Patient/attcp49

Immediate stabilization priorities

›Airway and respiratory threats

›Early respiratory failure from ascending paralysis

›Diaphragm and intercostal muscle involvement signals impending failure

›Forced vital capacity < 20 mL/kg is an intubation threshold

›Inability to clear secretions due to bulbar dysfunction

›Intubation triggers

›Declining GCS or bulbar signs

›SpO2 < 92% despite supplemental oxygen

›Rising PaCO2 with respiratory fatigue

›If intubating, use RSI; note autonomic lability may cause exaggerated BP response

›Ketamine acceptable as induction agent

›Succinylcholine carries theoretical hyperkalemia risk in denervated muscle

›Circulatory and autonomic threats

›Autonomic instability hallmark of clinical rabies

›Sinus tachycardia most common arrhythmia

›Labile blood pressure alternating hypertension and hypotension

›Bradycardia and heart block may occur

›Continuous cardiac monitoring mandatory in all suspected cases

›12-lead ECG on arrival

›Treat arrhythmias per standard ACLS protocol

›Vasopressor support for refractory hypotension

›Norepinephrine 0.05-0.5 mcg/kg/min titrated to MAP >= 65 mmHg

›Central venous access preferred for vasopressor administration

Team activation and consult triggers

›Immediate consultation requirements

›Infectious disease

›Rabies-specific diagnostics coordination

02History/hx72

Exposure history

›Animal contact details

›Species and behavior

›Dog bite globally accounts for 99% of human rabies deaths

›Bat exposure in the US — most common domestic source; bites may leave no visible marks

›Other: foxes, raccoons, skunks, coyotes, wolves

›Nature of exposure

›Bite (most common transmission route)

›Scratch with contaminated saliva

›Mucous membrane contact (eye, mouth, nose) with infectious material

›Wound characteristics

›Location relative to CNS — face and hand bites shorten incubation

›Depth and number of wounds

›Provoked vs unprovoked attack — unprovoked raises suspicion for rabid animal

›Geographic and temporal context

›Travel to endemic regions: South/Southeast Asia, Africa, Latin America

›Time since exposure — incubation typically weeks to months, range 7 days to years

›Bat cave exposure or spelunking

›PEP and vaccination history

›Prior PEP received

›Completeness of vaccine series

›HRIG given at time of exposure

›PEP failures documented with protocol deviations

›Pre-exposure prophylaxis

›Veterinarians, animal handlers, laboratory workers, travelers to endemic regions

Prodromal and symptom timeline

›Prodromal phase features

›Pain, paresthesia, or pruritus at the bite site — earliest and most specific prodromal symptom

03Physical Exam/exam66

Vital signs and general appearance

›Hemodynamic profile

›Fever

›Present in most cases; distinguishes rabies from GBS which is typically afebrile

›Temperature > 38.5 C in context of ascending paralysis raises rabies concern

›Heart rate

›Sinus tachycardia most common

›Labile rate reflecting autonomic dysfunction

›Blood pressure

›Hypertension and hypotension may alternate

›Labile BP is an autonomic instability marker

›Respiratory rate

›Tachypnea suggesting impending respiratory failure

›Paradoxical breathing pattern indicating diaphragm weakness

›General appearance

›Level of consciousness

›Preserved early — key distinguishing feature of paralytic form

›Progressive decline toward coma as disease advances

›Agitation and anxiety level

›More prominent in furious rabies

›May overlap in later paralytic disease

Neurological examination

›Motor system

›Flaccid weakness pattern

›Begins in bitten extremity

›Ascending course to involve trunk and contralateral limbs

›Eventually bulbar and respiratory muscles

›Reflexes

04Differential Diagnosis/ddx51

Primary diagnostic mimics

›Guillain-Barre syndrome (most important mimic)

›ICD-10: G61.0

›Ascending flaccid paralysis nearly identical presentation

›Albuminocytologic dissociation in CSF differentiates from rabies pleocytosis

›Fever absent in GBS; present in rabies

›Fasciculations and myoedema absent in GBS

›Bladder incontinence more prominent in paralytic rabies

›IVIG treatment in suspected GBS can confound rabies serology

›Transverse myelitis

›ICD-10: G37.3

›Sensory level present in myelitis; absent in rabies

›Bladder dysfunction common to both

›MRI spinal cord abnormalities more pronounced in myelitis

›Acute disseminated encephalomyelitis (ADEM)

›ICD-10: G36.9

›Post-infectious demyelination may follow viral prodrome

›Multifocal white matter lesions on MRI

›Responds to immunosuppression; rabies worsened by immunosuppression

›Poliomyelitis and enteroviral anterior myelitis

›ICD-10: A80.9

›Asymmetric flaccid paralysis without sensory changes

›CSF pleocytosis overlaps; enteroviral PCR differentiates

›West Nile virus anterior myelitis: seasonal, mosquito exposure

Additional differential considerations

›Botulism

›ICD-10: A05.1

›Descending paralysis — opposite direction to paralytic rabies

05Laboratory Tests/lt66

Rabies-specific diagnostics

›Diagnostic coordination

›Contact state health department and CDC before ordering rabies-specific tests

›CDC Poxvirus and Rabies Branch: 404-639-1050

›Tests performed at CDC and select state laboratories

›Multiple specimens required simultaneously for optimal sensitivity

›Saliva RT-PCR (NAAT)

›Specimen collection

›Saliva collected via swab or spit

›Ideally collected in morning when viral load highest

›Performance characteristics

›Single sample sensitivity approximately 70%

›Serial samples sensitivity > 98%

›Lower sensitivity in paralytic vs furious form: negative saliva in 78% of paralytic cases vs 15% furious

›Negative single result does not exclude rabies — repeat serial samples essential

›Nuchal skin biopsy

›Technique

›Full-thickness 5-6 mm punch biopsy from nape of neck containing hair follicles

›Submitted for DFA (direct fluorescent antibody) for rabies antigen in cutaneous nerve fibers

›Performance

›Nearly 100% sensitive when performed correctly

›Preferred confirmatory test ante-mortem

›Serum and CSF antibodies (RFFIT)

›Rapid fluorescent focus inhibition test — gold standard for neutralizing antibody

›CSF rabies antibody in an unvaccinated patient virtually confirms diagnosis

›Serum antibody alone less specific (may reflect prior vaccination)

›Antibody may not appear until late in disease course

06Diagnostic Tests/dt65

Scoring Systems

›No validated scoring system specific to paralytic rabies exists

›Clinical suspicion index

›Exposure history + ascending paralysis + fever = high suspicion

›Myoedema or fasciculations + bite-site paresthesias = highly specific findings

›Preserved consciousness early in ascending paralysis distinguishes from furious form

›GBS-Rabies Differentiation Score (clinical heuristic)

›Fever at presentation: favors rabies

›Bladder incontinence: favors rabies

›Fasciculations present: favors rabies

›CSF pleocytosis: favors rabies

›Albuminocytologic dissociation in CSF: favors GBS

›Preceding GI/respiratory illness: favors GBS

›Autonomic Instability Score (informal ICU monitoring)

›Heart rate lability, BP swings, hypersalivation, piloerection each scored

›Higher burden of autonomic features increases rabies probability

›ICD-10 code for rabies: A82.0 (sylvatic rabies), A82.1 (urban rabies), A82.9 (rabies unspecified)

MRI

›Brain MRI findings in paralytic rabies

›Standard sequences

›T2/FLAIR: Mild signal changes in brainstem, hippocampus, hypothalamus, or spinal cord

›DWI: Restricted diffusion may be seen in affected brainstem and gray matter

›Gadolinium: Typically absent enhancement — distinguishes from most other encephalitides

›Clinical significance

›MRI often appears normal or near-normal in early paralytic rabies

›Normal MRI does not exclude rabies

›Absence of enhancement on T1+Gad is characteristic and helpful

›Spinal cord MRI

07Disposition/dispo33

ICU admission criteria

›All confirmed or strongly suspected clinical rabies

›ICU admission without exception

›Continuous cardiac monitoring for arrhythmias

›Mechanical ventilation readiness

›Vasopressor access

›Neurology and infectious disease mandatory consultations

›Shared decision-making for experimental therapies

›Early palliative care integration

›Infection control precautions

›Standard precautions sufficient for healthcare workers

›Avoid mucosal or wound exposure to patient saliva or neural tissue

›Rabies not transmitted by casual contact, respiratory droplets, or fomites

Transfer considerations

›Indications for transfer to tertiary center

›Experimental treatment protocols (Milwaukee Protocol or variants)

›Available only at select academic centers

›Contact CDC for current trial availability

›Specialized rabies diagnostic capability

›Some state health labs perform testing; others require CDC referral

›Pediatric rabies

›Transfer to pediatric ICU with pediatric neurology support

Post-exposure (pre-symptomatic) patients

›Outpatient PEP management

›Wound care completed in ED; first vaccine dose given; HRIG infiltrated

›Patient scheduled for days 3, 7, 14 vaccine doses

›Written return precautions provided

›Return precautions for PEP patients

08Treatment/t86

Post-exposure prophylaxis (pre-symptomatic)

›Wound care (most critical first step)

›Irrigation technique

›Thorough wound washing with soap and water for minimum 15 minutes

›Alternatively povidone-iodine solution or 70% ethanol

›Reduces viral inoculation by up to 90%

›Wound management

›Delayed primary closure preferred — do not suture unless cosmetically or functionally necessary

›If suture required, infiltrate wound edges with HRIG before closing

›Tetanus prophylaxis per standard guidelines

›Human rabies immunoglobulin (HRIG)

›Imogam Rabies-HT or HyperRAB S/D

›Dose: 20 IU/kg total body weight

›Route: Infiltrate as much as anatomically feasible directly into and around wound

›Remainder of calculated dose injected IM at distant site (contralateral deltoid or thigh)

›Administered on day 0 only

›Can be given up to 7 days after first vaccine dose

›Previously vaccinated patients

›HRIG not indicated; active immunity present

›Give 2 doses of rabies vaccine only (days 0 and 3)

›Rabies vaccine schedule (unvaccinated)

›Imovax Rabies or RabAvert (HDCV or PCEC)

›1 mL IM (deltoid in adults; anterolateral thigh in children < 2 years)

›ACIP 4-dose schedule: days 0, 3, 7, 14

›Day 0 vaccine given at a different anatomical site from HRIG injection

›Immunocompromised patients

›5-dose schedule: days 0, 3, 7, 14, 28

›Serology 2 weeks after series completion to verify seroconversion

›RFFIT titre >= 0.5 IU/mL considered protective

Symptomatic (clinical rabies) supportive care

›Airway management

›Early intubation for impending respiratory failure

›RSI preferred; use ketamine 1.5-2 mg/kg IV as induction agent

›Etomidate 0.3 mg/kg IV as alternative

›Avoid succinylcholine if significant muscle denervation — risk of fatal hyperkalemia

›Rocuronium 1.2 mg/kg IV preferred paralytic

›Mechanical ventilation settings

›Lung-protective strategy: tidal volume 6-8 mL/kg IBW

›PEEP titrated to oxygenation target SpO2 92-96%

›Autonomic instability management

›Cardiovascular support

›Norepinephrine 0.05-0.5 mcg/kg/min for hypotension

›Titrate to MAP >= 65 mmHg

›Labetalol for hypertensive crises: 20 mg IV bolus, repeat every 10 min to 300 mg maximum

›Arrhythmia management

›Sinus tachycardia: treat underlying autonomic dysfunction

›Atropine 0.5-1 mg IV for symptomatic bradycardia

›External pacing if high-degree heart block

›Hypersalivation

›Glycopyrrolate 0.2 mg IV/SC every 4-6 hours to reduce secretions

›Scopolamine patch as alternative

›Seizure management

›First-line: lorazepam 0.05-0.1 mg/kg IV (maximum 4 mg per dose)

›May repeat after 5 minutes if seizure persists

›Second-line: levetiracetam 60 mg/kg IV over 15 minutes (maximum 4500 mg)

›Third-line: valproate sodium 40 mg/kg IV over 6 minutes

›Pain and sedation in ICU

›Analgesia: fentanyl infusion 25-100 mcg/hour, titrate to pain control

›Sedation: propofol 5-50 mcg/kg/min or midazolam 0.02-0.1 mg/kg/hour

›Target RASS -1 to -2 for comfort

Milwaukee Protocol (experimental)

›Historical context

›Therapeutic coma protocol first used in 2004 for Jeanna Giese case

›Single documented survival using this approach in bat-variant RABV

›Subsequent attempts largely unsuccessful, particularly for dog-variant RABV

›Components of original protocol

›Ketamine infusion: 2-3 mg/kg/hour to induce therapeutic coma

›Midazolam infusion: 0.05 mg/kg/hour continuous

›Amantadine 200 mg via NG tube twice daily

›Ribavirin 16 mg/kg IV loading dose then 8 mg/kg IV every 6 hours

›Current status

›Not considered standard of care

›Consider only at experienced centers after family/goals-of-care discussion

›Contact CDC for current experimental protocol availability

Palliative and comfort care

›Goals-of-care discussion

›Prognosis nearly universally fatal once clinical symptoms develop

›Average survival 11 days from symptom onset without ICU support

›Aggressive ICU care may extend to 1 month but outcome remains fatal

›Documented rare survivors exist but are exceptional

›Early family meeting with palliative care team

›Clarify goals: curative intent vs comfort measures

›Cultural and religious considerations

›Comfort-focused care

›Anxiolytic therapy for agitation and fear

›Midazolam 0.5-2 mg IV as needed for distress

›Haloperidol 1-5 mg IV for severe agitation

›Analgesics for bite-site or neuropathic pain

›Gabapentin 300-600 mg three times daily via NG tube

›Fentanyl patch or infusion for sustained pain control

09Special Populations/sp67

Pregnancy

›Maternal-fetal considerations

›Rabies in pregnancy

›PEP is not contraindicated in pregnancy — untreated rabies is nearly universally fatal

›HRIG is safe in pregnancy; no known teratogenicity

›Rabies vaccine (HDCV, PCEC) is safe in all trimesters per CDC and ACIP

›Fetal risk

›Rabies virus does not cross placenta under normal conditions

›No confirmed cases of transplacental transmission

›Maternal clinical rabies carries high fetal mortality from maternal death and hypoxia

›Clinical rabies in pregnancy

›ICU management identical to non-pregnant patients

›Airway management priority given reduced respiratory reserve

›Lateral decubitus positioning preferred after 20 weeks gestation

›Fetal monitoring with obstetrics consultation

›Medication safety

›Ketamine safe for induction in pregnancy

›Levetiracetam preferred anticonvulsant over valproate (teratogenic)

›Benzodiazepines: acceptable for seizure emergency; discuss fetal risks

›Palliative considerations

›Delivery timing discussion with maternal-fetal medicine

›Fetal viability assessment at gestational age

Geriatric

›Age-related risk modifications

›Exposure risk

›Domestic animal bites more common in older adults

›Delayed wound care presentation due to minimizing injury

›Atypical presentation risk

›Baseline cognitive impairment may mask early behavioral changes

›Delirium may be attributed to other causes

›PEP considerations

›PEP regimen unchanged in older adults

›Injection site: deltoid preferred; avoid gluteal injection (reduced immunogenicity)

›Consider comorbidities affecting immune response — ensure seroconversion

›Clinical rabies in older adults

›Respiratory failure

›Reduced respiratory reserve accelerates intubation requirement

›Baseline COPD or restrictive lung disease compounds weakness

›Cardiovascular

›Baseline CAD increases arrhythmia risk from autonomic instability

›Beta-blocker interactions with autonomic surges

›Goals-of-care

›Earlier palliative care discussion given comorbidity burden

›Advance directives review

Pediatrics

›Epidemiological considerations

›Children at higher risk due to unreported animal contact

›Lower bite wounds relative to body height increase exposure to dogs

›Facial and scalp bites more common in children — shorter incubation

›Children less likely to report minor bites or scratches

›Bat exposure during sleep

›Child found with bat in room — provide PEP regardless of visible marks

›PEP dosing in children

›HRIG: 20 IU/kg (identical weight-based dosing to adults)

›Infiltrate into wound; remainder given IM in anterolateral thigh

›Rabies vaccine: 1 mL IM regardless of age

›Anterolateral thigh in children < 2 years

›Deltoid in children >= 2 years

›4-dose schedule: days 0, 3, 7, 14 (identical to adults)

›Clinical rabies in children

›Seizure management weight-based

›Lorazepam 0.05-0.1 mg/kg IV (maximum 4 mg per dose)

›Levetiracetam 60 mg/kg IV (maximum 4500 mg or 2500 mg in children)

›Intubation

›RSI with ketamine 1.5-2 mg/kg IV

›Cuffed ETT preferred in children >= 8 years; uncuffed in younger children

›Tube size estimation: (age/4) + 4 for uncuffed, (age/4) + 3.5 for cuffed

›Milwaukee Protocol

›Only case of survival with Milwaukee Protocol was a child (Jeanna Giese, 15 years)

›Consider in pediatric patients at experienced centers

10Background/b81

Epidemiology

›Global burden

›Incidence and mortality

›Approximately 59,000 human rabies deaths annually worldwide

›Greater than 95% occur in Asia and Africa

›Dog bites account for 99% of global human rabies deaths

›Case fatality rate effectively 100% once clinical symptoms develop

›Domestic US epidemiology

›1-3 human rabies cases per year in the United States

›Bat variants responsible for majority of US cases

›Most US cases have no clear history of animal bite

›Paralytic form proportion

›Accounts for approximately 20-33% of all human rabies cases globally

›Higher proportion in areas where dog-variant RABV predominates

›Animal reservoir distribution

›Global: dogs remain primary vector

›Responsible for 99% of transmission to humans

›Elimination campaigns in Asia and Africa are primary WHO focus

›North America: wildlife reservoirs

›Bats: all US states; silver-haired and tricolored bat variants most common cause of human disease

›Raccoons: eastern US

›Skunks: north-central US and California

›Foxes: Alaska, Arizona, Texas

›Coyotes: Texas border region

›Transplant-transmitted rabies

›Rare clusters from undiagnosed donors

›Cornea, kidney, liver, vascular graft transmission documented

Pathophysiology

›Viral entry and peripheral nervous system transport

›Route of infection

›Lyssavirus (RABV) introduced through bite wound into muscle

›Initial replication in myocytes at inoculation site

›Binds to nicotinic acetylcholine receptors, NCAM, and p75 neurotrophin receptors on nerve terminals

›Retrograde axonal transport

›Virus hijacks dynein motor proteins for retrograde axonal transport

›Transport rate approximately 8-20 mm/day

›Explains incubation period inversely proportional to bite-to-brain distance

›CNS invasion and neuropathology

›Brainstem and spinal cord tropism in paralytic form

›Preferential infection of spinal cord anterior horn cells and dorsal root ganglia

›Perivascular inflammation and neuronophagia

›Negri bodies: eosinophilic cytoplasmic inclusions in hippocampal neurons and Purkinje cells — pathognomonic but may be absent in paralytic form

›Axonal Guillain-Barre-like pathology

›Paralytic rabies shows immune-mediated axonal injury in peripheral nerves

›Anti-GM1 and anti-GD1a ganglioside antibodies detected in some cases

›Suggests molecular mimicry between RABV antigens and peripheral nerve components

›Why the paralytic form occurs

›Paralytic vs furious form determinants

›Viral strain: bat variants and some dog strains preferentially produce paralytic form

›Host immune response: stronger early immune activation may modulate limbic involvement

›Route of transmission: hematogenous vs neural spread may favor different patterns

›Preserved consciousness mechanism

›Less involvement of limbic system and brainstem arousal circuits early

›Cortical involvement occurs late as virus spreads via centrifugal dissemination

›Autonomic dysfunction mechanism

›Hypothalamic and brainstem nuclei invasion

›Dysregulation of sympathetic and parasympathetic outflow

›Catecholamine surges causing cardiac arrhythmias

›Hypersalivation from excessive parasympathetic tone

Therapeutic Considerations

›PEP efficacy and timing

›PEP is nearly 100% effective when given promptly after exposure

›No documented PEP failures when correctly administered and begun promptly

›Failures occur with delayed wound care, deviation from schedule, or incorrect HRIG infiltration

›Single-visit PEP (1 dose vaccine + HRIG) being studied as simplified protocol

›PEP effectiveness window

›PEP must begin before CNS entry — once virus reaches CNS it is inaccessible to antibody

›No upper time limit for starting PEP after exposure but earlier is always better

›Why treatment fails for clinical disease

›Blood-brain barrier impermeability

›Passive antibody (HRIG, IVIG) cannot penetrate CNS once virus is established there

›Antiviral agents have poor CNS penetration

›Immune evasion

›RABV glycoprotein induces apoptosis of T lymphocytes

›Virus maintains axonal transport even in presence of systemic antibody

›Milwaukee Protocol limitations

›Theoretical basis: suppress limbic excitability, allow immune clearance

›Documented survival rate remains < 5% in published cases

›Dog-variant RABV appears less responsive than bat-variant

›Emerging therapies under investigation

›Monoclonal antibody combinations targeting RABV glycoprotein

›RVA122 and CR57 combination in animal models

›Favipiravir: broad-spectrum RNA polymerase inhibitor studied in animal models

›Intrathecal passive immunization: bypasses BBB; limited human data

11Patient Discharge Instructions/pdi32

copy discharge instructions

›Rabies post-exposure prophylaxis instructions

›You received the first dose of rabies vaccine and rabies immune globulin today

›This treatment is highly effective at preventing rabies if started promptly after exposure

›You must return for your remaining vaccine doses on the scheduled dates

›Your vaccine schedule

›Day 3 appointment

›Day 7 appointment

›Day 14 appointment

›Missing a dose reduces protection — contact your doctor immediately if you cannot attend

›Wound care at home

›Keep the bite wound clean and dry

›Wash the area gently with soap and water twice daily

›Watch for signs of infection: increasing redness, warmth, swelling, pus

›Return to the emergency department immediately if you develop

›Numbness, tingling, or pain at the bite site

›Weakness in any limb

›Difficulty swallowing or breathing

›Fever above 38.5 degrees C

›Behavioral changes, confusion, or agitation

›Difficulty drinking water or abnormal fear of water

›Animal reporting

›If the animal is a pet, ensure it is quarantined and observed for 10 days

›If it is a wild animal or stray, report to animal control immediately

›Do not handle or kill the animal yourself; capture if safe and report to authorities

›Important information about rabies

›Rabies is preventable with the vaccine series if treatment starts before symptoms develop

›Once symptoms appear, rabies becomes nearly always fatal — this is why completing PEP is critical

12References/r31

Guidelines and key sources

›Primary clinical references

›Hemachudha T, Ugolini G, Wacharapluesadee S, et al. Human Rabies: Neuropathogenesis, Diagnosis, and Management. Lancet Neurology. 2013. PMID 23602163

›Definitive review of paralytic rabies clinical features, diagnosis, and outcomes

›Source for 20-33% paralytic proportion and survival statistics

›Jackson AC. Rabies: A Medical Perspective. Revue Scientifique et Technique. 2018. PMID 30747124

›Comprehensive management perspective including PEP protocols

›Hemachudha T, Laothamatas J, Rupprecht CE. Human Rabies: A Disease of Complex Neuropathogenetic Mechanisms and Diagnostic Challenges. Lancet Neurology. 2002. PMID 12849514

›Foundational pathophysiology review

›Epidemiology and vaccine guidelines

›Rupprecht CE, Briggs D, Brown CM, et al. Use of a Reduced (4-Dose) Vaccine Schedule for Postexposure Prophylaxis. MMWR Recommendations and Reports. 2010. PMID 20300058

›ACIP 4-dose PEP schedule recommendation source

›Rao AK, Briggs D, Moore SM, et al. Use of a Modified Preexposure Prophylaxis Vaccination Schedule. MMWR. 2022. PMC 9098245

›Updated pre-exposure prophylaxis schedule

›Wallace RM, Shlim DR. Rabies. CDC Yellow Book. 2025

›Current US travel medicine and exposure management guidance

›Diagnostic and special studies

›Gadre G, Satishchandra P, Mahadevan A, et al. Rabies Viral Encephalitis: Clinical Determinants in Diagnosis With Special Reference to Paralytic Form. JNNP. 2010. PMID 19965838

›Clinical differentiation of paralytic rabies from GBS

›Sheikh KA, Ramos-Alvarez M, Jackson AC, et al. Overlap of Pathology in Paralytic Rabies and Axonal Guillain-Barre Syndrome. Annals of Neurology. 2005. PMID 15852372

›Shared immune-mediated axonal pathology in paralytic rabies and GBS

›Miller JM, Binnicker MJ, Campbell S, et al. Guide to Utilization of the Microbiology Laboratory for Diagnosis of Infectious Diseases: 2024 Update. IDSA/ASM. Clinical Infectious Diseases. 2024

›Laboratory test selection and interpretation guidance

›Recent case reports and outbreak data

›Blackburn D, Minhaj FS, Al Hammoud R, et al. Human Rabies - Texas, 2021. MMWR. 2022. PMID 36480462

›Recent US domestic rabies case illustrating diagnostic challenges

›Deschamps N, Mayence C, Parize P, et al. Paralytic Rabies Outbreak Mimicking Guillain-Barre Syndrome in French Amazonia. PLoS Neglected Tropical Diseases. 2026. PMID 41911281

›Cluster demonstrating GBS mimicry and diagnostic pitfalls

Evidence & Review