Rift Valley Fever

Also known as: RVF

Rift Valley fever is a viral hemorrhagic fever caused by a phlebovirus, endemic to parts of sub-Saharan Africa and the Arabian Peninsula, primarily affecting livestock (with associated significant agricultural and economic impact during outbreaks) but capable of causing human infection and, periodically, significant human outbreaks.

Transmission occurs through mosquito bites, or, more commonly in human cases during livestock outbreaks, through direct contact with the blood, body fluids, or tissues of infected animals, which is why abattoir workers, veterinarians, and herders are at particularly elevated risk during epizootic periods.

The large majority of human infections are asymptomatic or cause a mild, self limiting febrile illness, and it is this mild presentation that accounts for most cases, with severe disease occurring in only a small minority.

The typical mild illness presents with fever, headache, myalgia, and malaise, generally resolving within a week without specific treatment.
A small proportion of patients progress to more severe complications, which define the clinically important minority of cases: ocular disease, with retinal lesions that can cause permanent visual impairment, typically becoming apparent one to three weeks after the initial illness; hemorrhagic fever, with jaundice, bleeding manifestations, and hepatic involvement, carrying significant mortality; and encephalitis, presenting with confusion, seizures, or focal neurological deficit, typically occurring somewhat later in the illness course than the hemorrhagic complications.

Diagnosis is confirmed through RT-PCR detection of viral RNA, most sensitive early in the illness during the viremic phase.
Serology (IgM and IgG) supports diagnosis, particularly useful once the acute viremic window has passed, with IgM indicating recent infection.
FBC and LFTs support assessment of severity, particularly relevant in suspected hemorrhagic presentations, where thrombocytopenia and deranged liver function may be present alongside coagulopathy.
A relevant epidemiological context, livestock exposure, residence in or travel to an endemic or outbreak affected area, is an essential part of the diagnostic picture given the non-specific nature of the illness in isolation.

Differentials include other viral hemorrhagic fevers, malaria, and other causes of an acute febrile illness, with the specific epidemiological exposure context helping to narrow this differential considerably.

No specific antiviral treatment is established, and management is entirely supportive.

Mild disease requires only symptomatic treatment: rest, hydration, and antipyretics or analgesics, avoiding NSAIDs and aspirin where a hemorrhagic complication cannot yet be excluded, given the bleeding risk these agents carry.
Severe hemorrhagic disease requires the same principles of supportive care applied to other viral hemorrhagic fevers: careful fluid and electrolyte management, blood product support for significant bleeding or coagulopathy, and close monitoring for progression, generally in a higher level care setting.
Ocular involvement requires ophthalmological assessment and follow up, given the risk of permanent visual impairment from retinal lesions.
Encephalitis is managed supportively, following general principles applicable to viral encephalitis of other causes.
Prevention centers on vector control, personal protective measures against mosquito bites in endemic and outbreak affected areas, and, critically, appropriate protective equipment and precautions for those handling livestock or animal tissues during outbreak periods, alongside livestock vaccination programs (used in animals rather than routinely in humans, given that human vaccines remain primarily investigational or reserved for specific high risk occupational groups in some settings) as part of broader One Health outbreak control efforts.

Referral: infectious disease or tropical medicine input for confirmed or suspected cases, particularly severe presentations; ophthalmology for any suspected ocular involvement; public health notification given the outbreak potential and the need for coordinated human and veterinary public health response.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Meningitis

Meningitis is inflammation of the meninges, the membranes surrounding the brain and spinal cord, most commonly infectious (bacterial, viral, tuberculous, or fungal, each covered in further detail in their own dedicated entries) but occasionally non-infectious (drug-induced, malignant, or autoimmune).

This entry provides the general framework for recognition, workup, and initial approach; see the Meningococcal Meningitis, Haemophilus Meningitis, Neonatal Meningitis, Viral Meningitis, and Tuberculous Meningitis entries for pathogen-specific detail.

The classic triad of fever, neck stiffness, and altered mental status is present in only a minority of adult cases when all three are required simultaneously, and its absence should never be used to exclude the diagnosis, particularly in the very young, elderly, or immunocompromised, where presentation is frequently atypical or subtle.headache, photophobia, nausea and vomiting, and, in more severe or advanced disease, seizures and focal neurological deficits are common accompanying features.

Kernig's sign (pain and resistance on passive knee extension with the hip flexed) and Brudzinski's sign (involuntary hip and knee flexion on passive neck flexion) support the diagnosis when present but have limited sensitivity and should not be relied upon to exclude meningitis if negative.

A non-blanching petechial or purpuric rash strongly suggests meningococcal disease specifically (see that entry) and should prompt immediate empirical treatment without any diagnostic delay.

Lumbar puncture with CSF analysis is the definitive diagnostic investigation, assessing opening pressure, cell count and differential, protein, glucose (paired with a simultaneous serum glucose for comparison), Gram stain, and culture, with the specific pattern helping distinguish bacterial (neutrophilic pleocytosis, elevated protein, low CSF:serum glucose ratio, typically under 0.4) from viral (lymphocytic pleocytosis, normal or mildly elevated protein, normal glucose) causes, though overlap and atypical patterns occur, particularly early in the illness course or with partially treated bacterial meningitis
CT head before lumbar puncture is indicated where there are specific risk factors for raised intracranial pressure or an alternative structural cause (focal neurological deficit, papilledema, new-onset seizure, significantly reduced GCS, or immunocompromise) given the risk of coning with LP in this context, but should not delay empirical antibiotic administration, which should be given first if there is any anticipated delay to LP
Blood cultures should always be taken, ideally before antibiotics if this causes no meaningful delay, given a meaningful proportion of cases have positive blood cultures even where CSF culture is negative or LP is delayed or contraindicated
PCR-based multiplex meningitis/encephalitis panels, where available, offer rapid, sensitive pathogen identification across a broad range of bacterial and viral causes simultaneously

Empirical antibiotics should be given immediately on clinical suspicion, without waiting for LP or imaging if either would cause meaningful delay (a widely used benchmark is within 1 hour of presentation): a commonly used adult empirical regimen is IV ceftriaxone 2 g bd, with IV amoxicillin/ampicillin 2 g every 4 hours added in those at risk of Listeria monocytogenes (age over 50, pregnancy, immunocompromise, alcohol use disorder), since cephalosporins do not reliably cover Listeria
Dexamethasone (10 mg IV qds in adults, or 0.15 mg/kg IV every 6 hours in children), given with or just before the first antibiotic dose, is recommended for suspected or confirmed bacterial meningitis given evidence of reduced neurological sequelae, most robust for pneumococcal and Haemophilus meningitis specifically, and generally continued for 4 days if bacterial meningitis is confirmed, stopped if an alternative or non-bacterial cause is subsequently identified
Once a specific organism is identified, antibiotic therapy is rationalized per organism and sensitivity (see the Meningococcal Meningitis and Haemophilus Meningitis entries for pathogen-specific detail)
Supportive care includes careful fluid management (avoiding both hypovolemia and excessive fluid administration given the risk of cerebral edema), seizure management if present, and close neurological observation for signs of raised intracranial pressure or evolving complications (hydrocephalus, cerebral abscess, venous sinus thrombosis)
Public health notification is required for confirmed or strongly suspected bacterial meningitis in most jurisdictions, given the outbreak potential of certain causative organisms (see Meningococcal Meningitis entry specifically)

Referral: this is a medical emergency requiring immediate infectious disease and, where relevant, neurology or neurosurgery involvement; ICU for reduced consciousness, seizures, or hemodynamic instability.

Rift Valley Fever

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management