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Reliable, easy-to-read patient information on common medical conditions — written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.

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Rabies differential diagnosis

Introduction

Overview

Overview

The differential diagnosis for rabies deals with eliminating diseases with similar symptoms from the diagnosis. There are many viruses that can appear similar to rabies such as encephalitis and the herpes simplex virus. It is very important to rule out certain diseases such as echovirus and poliovirus. Rabies is a serious disease that needs to be treated quickly if someone is suspected to be infected with the virus.

Differentiating Rabies From Other Diseases

Differentiating Rabies From Other Diseases

Rabies should be differentiated from other causes of headache and decrease consciousness:

Diseases History and Physical Diagnostic tests Other Findings
Prodromal symptoms Fever Headache LOC Neuro Onset Laboratory Findings Imaging preferance
Rabies infection[1] + + + + Insidious Antibody detection in serology

Skin biopsy of injured skin

MRI Hydrophobia, aerophobia, dysphagia, and localized pain, weakness or paresthesias
Meningitis[2][3] + + + – Sudden CSF analysis:

↑ Leukocytes

↑ Protein

↓ Glucose

CT scan: First choice

MRI: Best choice

Fever, neck, rigidity
Encephalitis[4] + + + + Sudden PCR

CSF analysis and culture reveal the responsible micro-organism

MRI Accompany a meningoencephalitis, seizures, hemiparesis, cranial nerve palsies, photophobia, nausea
Autoimmune encephalitis[5] – +/- + +/- Insidious Autoantibodies present in both serum and CSF MRI

EEG

Memory deficit, dyskinesias, seizures, autonomic instability
CNS abscess[6] + + + + Insidious CSF analysis:

↑ Leukocytes

↓ Glucose

↑ Protein

MRI is more sensitive and specific High grade fever, fatigue,nausea, vomiting
Poliomyelitis[7] + + + + Sudden PCR of CSF MRI Asymmetric paralysis following a flu-like syndrome
Neurosyphilis[8] – – + + Insidious CSF VDRL-specifc

CSF FTA-Ab -sensitive

MRI & Lumbar puncture History of unprotected sex or multiple sexual partners, and genital ulcer (chancre)

Blindness, confusion, depression, abnormal gait

Tick paralysis (Dermacentor tick)[9] – – +/- +/- Insidious – – History of outdoor activity in Northeastern United States

Tick often still latched to the patient at presentation (often in head and neck area)

Botulism[10] – – – – Sudden Toxin test, blood, wound, or stool culture – Diplopia, Hyporeflexia, Hypotonia, possible respiratory paralysis, Floppy baby syndrome
Tetrodotoxin poisoning[11] – – +/- +/- Sudden – – History of consumption of puffer fish species
Metabolic disturbances (electrolyte imbalance, hypoglycemia)[12] – +/- – + Sudden Hypoglycemia, hypo and hypernatremia MRI Confusion, seizure, palpitations, sweating, dizziness, hypoglycemia
Electrolyte disturbance[13] – – – +/- Insidious Hypocalcemia, hypomagnesemia, hypo- or hyperkalemia Possible arrhythmia
Drug toxicity/Neuroleptic malignant syndrome[14] – + – + Sudden Elevated serum creatine kianse

Hypocalcemia, hypomagnesemia, hypo- and hypernatremia, hyperkalemia, and metabolic acidosis

Generalized slow wave EEG Causative medications (eg, neuroleptics, antiemetics, concomitant lithium), dopaminergic withdrawal

Mental status change, rigidity, or dysautonomia

Organophosphate toxicity[15] – – – + Sudden Clinical suspicion confirmed with RBC AchE activity – History of exposure to insecticide or living in farming environment with : Diarrhea, Miosis, Bradycardia, Lacrimation, Emesis, Salivation, Sweating
Ischemic stroke[16] – – +/- + Sudden – MRI for ischemia Sudden unilateral motor and sensory deficit in a patient with a history of atherosclerotic risk factors (diabetes, hypertension, smoking) or atrial fibrillation
Hemorrhagic stroke[17] – – + + Sudden – CT scan without contrast Neck stiffness
Subdural hemorrhage[18] – – + + Sudden CSF analysis:

Xanthochromia

CT scan without contrast Confusion, dizziness, nausea, vomiting
Hypertensive encephalopathy[19] – – + + Sudden – – Delirium, cortical blindness, cerebral edema, seizure
Wernicke’s encephalopathy[20] – – – + Sudden – – Ophthalmoplegia, confusion
Amyotrophic lateral sclerosis[21] – – +/- +/- Insidious Normal LP (to rule out DDx) MRI Patient initially presents with upper motor neuron deficit (spasticity) followed by lower motor neuron deficit (flaccidity)
Diffuse gliomatosis[22] – – + – Insidious Cancer specific molecular characteristics

Normal CSF

MRI (expansile, T2 hyperintense lesion) Seizures, memory loss, motor weakness, visual symptoms, language deficit, and cognitive and personality changes
Central nervous system lymphoma[23] + – + +/- Insidious CSF cytology, flow cytometry, and stereotactic brain biopsy MRI (parenchymal or leptomeningeal enhancement) Associated with immunodeficiency

Focal neurological deficits, neuropsychiatric symptoms, signs of raised intracranial pressure, seizures, and ocular symptoms

The most important differential diagnosis when it comes to the rabies presentations include meningitis and encephalitis. It is important to differentiate different rabies from each one of the causes of meningitis/encephalitis, which may differ based on the season of occurrence and the geographical region.

The most important viruses to rule out are:[24][25]

In addition, consideration should be given to the local epidemiology of encephalitis caused by arboviruses belonging to several taxonomic groups, including:

New causes of viral encephalitis are also possible, as was evidenced by the recent outbreak in Malaysia of some 300 cases of encephalitis (mortality rate, 40%) caused by Nipah virus, a newly recognized paramyxovirus. Similarly, well-known viruses may be introduced into new locations, as is illustrated by the recent outbreak of encephalitis due to West Nile virus in the eastern United States. Epidemiological factors (e.g., season, geographic location, and the patient’s age, travel history, and possible exposure to animal bites, rodents, and ticks) may help direct the diagnostic workup.

References

References

  1. ↑ Baevsky RH, Bartfield JM (1993). “Human rabies: a review”. Am J Emerg Med. 11 (3): 279–86. PMID 8489675.
  2. ↑ Tacon CL, Flower O (2012). “Diagnosis and management of bacterial meningitis in the paediatric population: a review”. Emerg Med Int. 2012: 320309. doi:10.1155/2012/320309. PMC 3461291. PMID 23050153.
  3. ↑ Chadwick DR (2005). “Viral meningitis”. Br. Med. Bull. 75-76: 1–14. doi:10.1093/bmb/ldh057. PMID 16474042.
  4. ↑ Steiner I, Budka H, Chaudhuri A, Koskiniemi M, Sainio K, Salonen O, Kennedy PG (2005). “Viral encephalitis: a review of diagnostic methods and guidelines for management”. Eur. J. Neurol. 12 (5): 331–43. doi:10.1111/j.1468-1331.2005.01126.x. PMID 15804262.
  5. ↑ Lancaster E (2016). “The Diagnosis and Treatment of Autoimmune Encephalitis”. J Clin Neurol. 12 (1): 1–13. doi:10.3988/jcn.2016.12.1.1. PMC 4712273. PMID 26754777.
  6. ↑ Alvis Miranda H, Castellar-Leones SM, Elzain MA, Moscote-Salazar LR (2013). “Brain abscess: Current management”. J Neurosci Rural Pract. 4 (Suppl 1): S67–81. doi:10.4103/0976-3147.116472. PMC 3808066. PMID 24174804.
  7. ↑ Obregón R, Chitnis K, Morry C, Feek W, Bates J, Galway M, Ogden E (2009). “Achieving polio eradication: a review of health communication evidence and lessons learned in India and Pakistan”. Bull. World Health Organ. 87 (8): 624–30. PMC 2733260. PMID 19705014.
  8. ↑ Timmermans M, Carr J (2004). “Neurosyphilis in the modern era”. J. Neurol. Neurosurg. Psychiatr. 75 (12): 1727–30. doi:10.1136/jnnp.2004.031922. PMC 1738873. PMID 15548491.
  9. ↑ Edlow JA, McGillicuddy DC (2008). “Tick paralysis”. Infect. Dis. Clin. North Am. 22 (3): 397–413, vii. doi:10.1016/j.idc.2008.03.005. PMID 18755381.
  10. ↑ Cherington M (2004). “Botulism: update and review”. Semin Neurol. 24 (2): 155–63. doi:10.1055/s-2004-830901. PMID 15257512.
  11. ↑ Hwang DF, Noguchi T (2007). “Tetrodotoxin poisoning”. Adv. Food Nutr. Res. 52: 141–236. doi:10.1016/S1043-4526(06)52004-2. PMID 17425946.
  12. ↑ Josephson MA, Kaul S, Hopkins J, Kvam D, Singh BN (1985). “Hemodynamic effects of intravenous flecainide relative to the level of ventricular function in patients with coronary artery disease”. Am. Heart J. 109 (1): 41–5. PMID 3966331.
  13. ↑ Marcelou-Kinti O, Velegraki-Abel A (1988). “[Resistance to amphotericin B and genotypic resistance to 5-fluorocytosine of serotypes A and B of Candida albicans]”. Therapie (in French). 43 (2): 121–2. PMID 3043756.
  14. ↑ Pelonero AL, Levenson JL, Pandurangi AK (1998). “Neuroleptic malignant syndrome: a review”. Psychiatr Serv. 49 (9): 1163–72. doi:10.1176/ps.49.9.1163. PMID 9735957.
  15. ↑ Minton NA, Murray VS (1988). “A review of organophosphate poisoning”. Med Toxicol Adverse Drug Exp. 3 (5): 350–75. PMID 3057326.
  16. ↑ Baldwin K, Orr S, Briand M, Piazza C, Veydt A, McCoy S (2010). “Acute ischemic stroke update”. Pharmacotherapy. 30 (5): 493–514. doi:10.1592/phco.30.5.493. PMID 20412000.
  17. ↑ Bullard CW (1987). “Issues in low-level radioactive waste management”. JAPCA. 37 (11): 1337–41. PMID 3443867.
  18. ↑ Cenic A, Bhandari M, Reddy K (2005). “Management of chronic subdural hematoma: a national survey and literature review”. Can J Neurol Sci. 32 (4): 501–6. PMID 16408582.
  19. ↑ Schwartz RB (2002). “Hyperperfusion encephalopathies: hypertensive encephalopathy and related conditions”. Neurologist. 8 (1): 22–34. PMID 12803657.
  20. ↑ Flynn A, Macaluso M, D’Empaire I, Troutman MM (2015). “Wernicke’s Encephalopathy: Increasing Clinician Awareness of This Serious, Enigmatic, Yet Treatable Disease”. Prim Care Companion CNS Disord. 17 (3). doi:10.4088/PCC.14r01738. PMC 4578911. PMID 26644959.
  21. ↑ Zarei S, Carr K, Reiley L, Diaz K, Guerra O, Altamirano PF, Pagani W, Lodin D, Orozco G, Chinea A (2015). “A comprehensive review of amyotrophic lateral sclerosis”. Surg Neurol Int. 6: 171. doi:10.4103/2152-7806.169561. PMC 4653353. PMID 26629397.
  22. ↑ Chen S, Tanaka S, Giannini C, Morris J, Yan ES, Buckner J, Lachance DH, Parney IF (2013). “Gliomatosis cerebri: clinical characteristics, management, and outcomes”. J. Neurooncol. 112 (2): 267–75. doi:10.1007/s11060-013-1058-x. PMC 3907195. PMID 23341100.
  23. ↑ Wilne SH, Ferris RC, Nathwani A, Kennedy CR (2006). “The presenting features of brain tumours: a review of 200 cases”. Arch. Dis. Child. 91 (6): 502–6. doi:10.1136/adc.2005.090266. PMC 2082784. PMID 16547083.
  24. ↑ Romero JR, Newland JG (2003). “Viral meningitis and encephalitis: traditional and emerging viral agents”. Semin Pediatr Infect Dis. 14 (2): 72–82. doi:10.1053/spid.2003.127223. PMID 12881794.
  25. ↑ Xie Y, Tan Y, Chongsuvivatwong V, Wu X, Bi F, Hadler SC, Jiraphongsa C, Sornsrivichai V, Lin M, Quan Y (2015). “A Population-Based Acute Meningitis and Encephalitis Syndromes Surveillance in Guangxi, China, May 2007-June 2012”. PLoS ONE. 10 (12): e0144366. doi:10.1371/journal.pone.0144366. PMC 4669244. PMID 26633824.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mahshid Mir, M.D. [2]