Viral haemorrhagic fevers

• Viral haemorrhagic fever is a syndrome, not one disease: arenaviruses (Lassa), filoviruses (Ebola, Marburg), bunyaviruses (Crimean-Congo haemorrhagic fever, Rift Valley fever, hantaviruses) and flaviviruses (yellow fever, dengue). Ebola, Marburg, Lassa and Crimean-Congo haemorrhagic fever are high consequence infectious diseases in the UK because they pass person to person.^[3]
• No specific curative drug for most. Management is optimised supportive care: fluids, electrolytes, blood products, treatment of co-infection, intensive care.^[1][4][5][6]
• Monoclonal antibodies (mAb114 50 mg per kg, or REGN-EB3 150 mg per kg, each a single intravenous infusion) reduce mortality in Ebola caused by Zaire ebolavirus when given early.^[2]
• Ribavirin is off-label with uncertain benefit in Crimean-Congo haemorrhagic fever and Lassa fever; intravenous ribavirin early decreases illness and death in haemorrhagic fever with renal syndrome.^[4][5][9]
• In the UK, an "at risk" patient is isolated in a single side room, malaria excluded first, VHF testing through the Imported Fever Service (6 to 8 hours after the specimen arrives), confirmed cases to a high level isolation unit (HLIU).^[3]

By the end of this page you should be able to:

1. Name the virus, reservoir and transmission route for Ebola and Marburg, Lassa, Crimean-Congo haemorrhagic fever, yellow fever, hantavirus and Rift Valley fever.
2. Recognise the syndrome each produces, including the two-phase course of yellow fever and the lung-kidney split in hantavirus disease.
3. Explain supportive management of Ebola and Marburg disease in a resource-limited unit, including balanced crystalloids, vasopressors and tranexamic acid.
4. State which monoclonal antibodies are recommended for Ebola caused by Zaire ebolavirus, with doses, and where ribavirin evidence is strong or weak.
5. Work through UK risk-assessment steps for a febrile traveller: the 21-day window, malaria screen, Imported Fever Service testing and HLIU transfer.
6. Outline notification, isolation, supportive care and prevention, including low-resource settings.

Viral haemorrhagic fevers are diseases students meet as outbreak headlines and doctors meet as a febrile, hypotensive traveller with an uncertain diagnosis. They are rare outside endemic areas but severe; some spread in hospital; all are easy to miss early. This page follows the WHO 2026 guideline on filovirus disease management, the UK Health Security Agency and ACDP 2026 algorithm, the WHO fact sheets for Crimean-Congo haemorrhagic fever, Lassa fever, Rift Valley fever and yellow fever, and the CDC clinician briefs for hantavirus pulmonary syndrome and haemorrhagic fever with renal syndrome. For vaccination and the wider arboviral differential see the mosquito-borne viruses page.

One habit underlies all: any acutely unwell patient with feverishness and a relevant travel or exposure history within the previous 21 days must be risk-assessed for viral haemorrhagic fever before a benign diagnosis is accepted. Malaria is commoner, but missing a haemorrhagic fever kills the patient and can infect staff.^[3]

A viral haemorrhagic fever is a severe multisystem illness caused by an enveloped RNA virus. Damage is driven by endothelial injury and increased vascular permeability, plus direct liver, kidney or lung infection with some agents. Bleeding is common but rarely the cause of death; shock, fluid loss and organ failure kill.

The viruses fall into four families: Arenaviridae (Lassa; rodents), Filoviridae (Ebola, Marburg; bats), Bunyaviridae (Crimean-Congo haemorrhagic fever, Rift Valley fever, hantaviruses; ticks, mosquitoes or rodents), Flaviviridae (yellow fever, dengue; mosquitoes). Two axes matter more than name: transmissibility (person-to-person spread dictates isolation) and severity (mild to fulminant).

• Ebola and Marburg disease: sub-Saharan Africa. Sporadic forest-adjacent outbreaks, amplified in hospitals. Ebolavirus has six species; three cause large outbreaks (Ebola, Sudan, Bundibugyo viruses); Taï Forest virus infection in humans is rarely documented. Case fatality varies by outbreak: about 50% on average for Ebola virus disease (range 25 to 90%) and for Marburg virus disease (range 24 to 88%). Marburg is clinically similar and similarly severe. The WHO 2026 guideline adds 16 recommendations, including for a Bundibugyo outbreak.^{[3][10][11] [4]}
• Lassa fever: West Africa (Benin, Ghana, Guinea, Liberia, Mali, Nigeria, Sierra Leone). Overall fatality 1%, but 15% or higher in hospitalised severe disease.^[5]
• Crimean-Congo haemorrhagic fever: Africa, Balkans, Middle East, Asia south of the 50th parallel north. Fatality 10 to 40%.^[4]
• Yellow fever: 27 African and 13 Latin American countries. Estimated 67 000 to 173 000 severe infections and 31 000 to 82 000 deaths yearly in Africa and the Americas.^[7]
• Hantavirus: worldwide. HPS kills about 38% of those with respiratory symptoms; HFRS kills 5 to 15% of Hantaan or Dobrava infections but under 1% of Seoul, Saaremaa or Puumala infections.^[8][9]
• Rift Valley fever: sub-Saharan Africa, Egypt, Saudi Arabia, Yemen after heavy rain and livestock movement. Human disease usually mild; haemorrhagic form fatal in about 50%.^[6]
• Brucellosis, leptospirosis, plague and Q fever: not VHFs, not transmissible person to person, not covered by the ACDP pathway; each has its own guidance. They mimic VHF early and should be considered.^[3]
• UK context: environmental conditions do not support the reservoirs. All but three recorded UK cases acquired abroad.^[3]

Risk is shaped by place, season and occupation: living in or travelling to an endemic area within 21 days; contact with livestock, slaughter, veterinary work; rodents; bats; tick and mosquito bites; healthcare or laboratory exposure; documented sexual transmission of Ebola up to 5 years after recovery.^[3] Severe disease is more likely in pregnancy, immunosuppression, extremes of age and co-infection. Lassa fever in pregnancy carries very high maternal and fetal mortality.^{[5] [6]}

1. Inoculation through mucous membranes, broken skin, bites or contaminated food.
2. Local replication then viraemia.
3. Endothelial dysfunction and vascular leak; direct organ infection; immune-mediated pulmonary leak in HPS.
4. Clinical expression: fever, leak, coagulopathy, organ dysfunction; bleeding late.
5. Recovery if supportive care bridges the leak.

Yellow fever exemplifies a two-phase illness: febrile viraemia, brief remission, then jaundice, bleeding and shock.^[7]

Travel and exposure first: where in the last 21 days; animal, tick, mosquito, rodent contact; cave or bat exposure; hospital or laboratory work; sick contacts; pregnancy and immune status; yellow fever vaccination.^[3]

Fever, tachycardia, prostration, flushing, conjunctival injection, pharyngitis, lymphadenopathy; rash; jaundice, hepatomegaly, pleural and peritoneal fluid, oedema; bleeding from gums, nose, gut, vagina; hypotension, shock, oliguria.

Incubation 2 to 21 days. Abrupt onset fever, headache, myalgia, sore throat then profuse watery diarrhoea, vomiting, abdominal pain with massive fluid loss. Rash around day 5. Late haemorrhagic signs in a minority. Oliguria, confusion, shock mark deterioration. Viral RNA can persist in semen for months.^[2][3]

About 80% asymptomatic or mild. Symptomatic illness starts gradually (fever, malaise, headache, sore throat, myalgia, chest pain, nausea, vomiting, diarrhoea) then severe disease brings facial swelling, fluid accumulation, bleeding, hypotension. Hearing loss up to 25% of survivors. Incubation 2 to 21 days. About 15% hospitalised die, usually within 14 days. In pregnancy late Lassa carries over 80% fetal loss and 30% maternal mortality.^[5]

Incubation 1 to 3 days after tick bite (max 9) or 5 to 6 days after tissue contact (max 13). Sudden fever, myalgia, dizziness, neck pain, backache, headache, photophobia, nausea, vomiting, diarrhoea, abdominal pain, then mood swings, confusion, lassitude. Hepatomegaly, tachycardia, lymphadenopathy, petechial rash, hepatitis. Kidney, liver or lung failure after day 5. Fatality about 30%, death in second week; recovery from day 9 to 10.^{[4] [7]}

Incubation 3 to 6 days; most mild. First phase 3 to 4 days of fever, headache, aches, nausea, vomiting, weakness. About 15% progress after brief remission to severe disease: returning fever, jaundice, bleeding, organ failure, shock; about half of severe cases die within 7 to 10 days.^[7]

• HPS. Incubation 1 to 8 weeks. Prodrome 3 to 5 days, then cough, breathlessness, chest tightness over hours, hypotension within 24 hours. Case-fatality about 38% of those developing respiratory symptoms. Deaths occur 24 to 48 hours after cardiopulmonary onset without intensive care.^[8]
• HFRS. Incubation 1 to 2 weeks (rarely up to 8). Sudden severe headache, back and abdominal pain, fever, chills, nausea, blurred vision, flushing, eye inflammation or rash, then hypotension, shock, vascular leak and acute kidney failure. Puumala/Seoul/Saaremaa milder (under 1% fatality); Hantaan/Dobrava severe (5 to 15%). Recovery weeks to months.^[9]

Incubation 2 to 6 days. Most asymptomatic or mild feverish illness lasting 4 to 7 days. Three severe forms: ocular (0.5 to 2%, retinal lesions, permanent vision loss in 50% when macula involved); meningoencephalitis (under 1%, onset 1 to 4 weeks later, residual deficits common, low fatality); haemorrhagic fever (under 1%, liver failure then haemorrhage, fatality about 50%, death 3 to 6 days after onset).^[6]

• FBC, clotting screen, urea and electrolytes, liver function tests, glucose, creatinine, CRP, urinalysis.
• Malaria screen (priority in the UK pathway, and wherever malaria possible).
• VHF PCR through the national laboratory (UK: Imported Fever Service/RIPL; USA: CDC Viral Special Pathogens Branch).
• Disease-specific PCR/serology.
• Imaging for pleural and peritoneal fluid; ECG; blood gases and lactate if shock.
• High biohazard: containment level 2 or higher, sealed transport, no pneumatic tubes, retain specimens until VHF status known.

In the UK, VHF results are usually available 6 to 8 hours after the laboratory receives the specimen, and RIPL tests in parallel for dengue, rickettsiae and leptospirosis. ^[3]

There is no single severity score across all these agents. In the UK the operational categories are "minimal risk", "at risk" and "confirmed" VHF.^[3] VHF is notifiable: suspected or confirmed HCID cases go through national public health systems, with contacts monitored 21 days after last exposure.^[3]

1. Risk assessment by a senior clinician plus infectious-disease or microbiology/virology. Any acutely unwell patient with feverishness and a travel or exposure history within 21 days.^[3]
2. Minimal risk: single side room, standard precautions; urgent malaria testing. If malaria positive and improving on treatment, VHF unlikely. If malaria negative and unwell with no diagnosis, escalate.
3. At risk: single side room immediately; unified HCID PPE (per the NIPCM HCID addendum); minimise movements; restrict visitors; FBC, U&E, LFTs, clotting, CRP, glucose, blood cultures, urgent malaria; discuss VHF testing with the Imported Fever Service (0844 778 8990) before sending samples; transport by category A or B courier.
4. Confirmed VHF: notify UKHSA, NHS England EPRR and the HLIU; transfer (usually road, occasionally air); restrict staff; keep a contact list; full public health actions including contact tracing, monitoring and possible post-exposure prophylaxis. HCID PPE throughout.

Key isolation principles: experts agree there is no circumstantial or epidemiological evidence of airborne transmission from VHF patients; transmission mainly by direct contact with blood and body fluids or indirect contact with contaminated environments. Precautionary approach for aerosol-generating procedures. Unwell VHF patients in a negative-pressure isolation suite (with or without bed isolator) within an HLIU.^[3]

The WHO 2026 guideline sets 16 evidence-based recommendations across monitoring, fluids, shock, bleeding and follow-up. Core points: ^[1]

• Systematic monitoring: structured, documented clinical assessment at regular intervals, frequency adapted to condition. Laboratory tests guided by clinical assessment rather than routine testing.^[1]
• Oral rehydration: protocolised oral rehydration (e.g. WHO Plan B) for patients with ongoing gastrointestinal fluid losses and some dehydration.^[1]
• Intravenous fluids: protocolised IV regimen for severe dehydration compared with no protocolised regimen; balanced crystalloids (such as Ringer's lactate) rather than 0.9% sodium chloride for acute IV resuscitation.^[1]
• Perfusion assessment: serial measurement of lactate and capillary refill time to guide fluid management in shock.^[1]
• Vasopressors: initiate early in shock; norepinephrine preferred over dopamine (and favoured over epinephrine). Peripheral catheter acceptable for initiation; ultrasound-guided placement if central access needed.^[1]
• Co-infection: presumptive broad-spectrum antibiotics where sepsis or bacterial co-infection suspected; not routine in low-likelihood patients. Antibiotic choice by local resistance; intravenous without delay.^[1]
• Haemorrhage: tranexamic acid suggested against in confirmed filovirus disease with haemorrhage, but suggested for in postpartum haemorrhage.^[1]
• Follow-up: structured follow-up after discharge for survivors.^[1]

• Ebola (Zaire ebolavirus): WHO 2022 therapeutics guideline makes a strong recommendation for mAb114 (ansuvimab, Ebanga) 50 mg per kg, or REGN-EB3 (atoltivimab + maftivimab + odesivimab; Inmazeb) 150 mg per kg, each as a single intravenous infusion over 60 minutes (mAb114) or 2 to 4 hours (REGN-EB3), given as soon as possible after RT-PCR confirmation. They should not be given together; choose on availability. Both reduce 28-day mortality versus standard care. Also recommended for neonates of unproven status 7 days old or younger born to mothers with confirmed Ebola. ZMapp and remdesivir are recommended against. All recommendations apply only to Zaire ebolavirus.^[2]
• Marburg: no specific approved antiviral. Supportive care; candidates in trials. Covered by the 2026 WHO filovirus guideline.
• Lassa fever: no approved antiviral. WHO fact sheet: ribavirin has been given, but considerable uncertainty about efficacy and optimal dosing; enrol patients in randomised trials whenever possible. Early intensive supportive care with rehydration and symptomatic treatment improves survival. No licensed vaccine.^[5]
• Crimean-Congo haemorrhagic fever: no specific approved treatment. Early intensive supportive care including fluid management can improve chances of survival. Ribavirin given off-label, but considerable uncertainty about efficacy and optimal dosing; if used, enrol into a randomised trial. No vaccine widely available (an inactivated mouse brain-derived vaccine used on a small scale in eastern Europe).^[4]
• Rift Valley fever: most human cases mild and self-limiting; no specific treatment. Severe cases receive early intensive supportive care including fluid management. An inactivated vaccine exists but is not licensed or commercially available; used experimentally for high-risk workers.^[6]
• Yellow fever: no specific antiviral; care supportive. Two antivirals (sofosbuvir and monoclonal antibody TY014) are recommended only in research settings. Jaundice indicates severe disease; hospitalise, often in intensive care. Yellow fever vaccine (single dose, lifelong) is the best prevention.^[7]
• Hantavirus: no specific treatment for HPS; immediate intensive care, careful fluids, oxygen, intubation/ventilation as needed; ECMO at first sign of decompensation has about 80% survival despite collapse; prognosis poor if plasma lactate above 4.0 mmol per L or cardiac index under 2.2 L per min per m2. For HFRS, supportive therapy and intravenous ribavirin early can decrease illness and death; dialysis may be needed for fluid overload.^[8][9]

Flowchart of the UK acute-hospital approach:

• For all agents: shock, acute kidney injury, liver failure, coagulopathy, bleeding, secondary bacterial infection, intensive-care complications.
• Ebola/Marburg: prolonged convalescence, persistence in semen, post-Ebola syndrome (uveitis, joint pain) not covered in detail here.
• Lassa: hearing loss in up to 25% of survivors; high maternal/fetal mortality in pregnancy.^[5]
• Crimean-Congo haemorrhagic fever: kidney, liver, lung failure after day 5; about 30% fatality.^[4]
• Yellow fever: jaundice, renal failure, shock; haemorrhage; death in about half of severe cases.^[7]
• HPS: rapid respiratory failure; death 24 to 48 hours after cardiopulmonary onset without intensive care; poor prognostic lactate and cardiac index.^[8]
• HFRS: acute kidney failure with fluid overload; weeks to months of recovery.^[9]
• Rift Valley fever: ocular form with permanent vision loss in 50% when macula involved; meningoencephalitis with long-term neurological deficits; haemorrhagic form.^[6]

Prognosis is determined by the agent, speed of recognition and quality of supportive care. With early, vigorous resuscitation, filovirus mortality can fall well below the historical averages. HPS and haemorrhagic Rift Valley fever carry the highest acute case-fatality (about 38% and about 50% respectively). Yellow fever severe cases carry about 50% fatality. Hantaan/Dobrava HFRS 5 to 15%. Lassa 15% or higher in hospitalised severe disease. Crimean-Congo about 30%. The general rule: the earlier the patient is recognised and supported, the better the outcome. ^[7]

• General: infection prevention and control (hand hygiene, PPE, safe injection, safe burial), standard plus transmission-based precautions, isolation and containment, contact tracing and 21-day monitoring.
• Individual protection: tick bite prevention for Crimean-Congo haemorrhagic fever (protective clothing, repellents, tick checks, acaricide use on animals prior to slaughter); mosquito bite prevention for yellow fever and Rift Valley fever (repellents, covering, nets); rodent avoidance and safe food storage for Lassa; glove use and safe handling of animal tissues.
• Vaccination:
  • Yellow fever: single dose gives lifelong immunity; not for infants under 9 months, pregnant women (except outbreaks), severe egg allergy, severe immunodeficiency. Risk-benefit above 60 years warrants care.^[7]
  • Rift Valley fever: an inactivated vaccine exists for high-risk workers but is not commercially licensed. Animal vaccination programs are the key control (must be given before outbreaks; not during outbreak because of needle/syringe reuse risks).^[6]
  • Crimean-Congo haemorrhagic fever: no safe, effective widely available vaccine (an inactivated, mouse brain-derived vaccine used on a small scale in eastern Europe).^[4]
  • Lassa fever: no licensed vaccine, several candidates in development.^[5]
  • Ebola: licensed vaccines exist for Zaire ebolavirus (e.g. Ervebo is WHO-prequalified); monoclonal antibodies are for treatment, not prophylaxis in routine practice.
• Rodent control central for Lassa and hantavirus (but Mastomys rats are ubiquitous and cannot be eliminated).
• Screening: there is no population screening programme. The practical equivalent is a travel and exposure history in every febrile illness and a low threshold for testing in returning travellers. Lassa fever diagnosis should be considered in febrile patients returning from West Africa. Hantavirus should be considered in anyone with compatible symptoms and rodent exposure.
• Nosocomial control: confirmed patients to HLIU; standard infection prevention and control precautions for CCHF, Lassa, RVF and hantavirus; extra contact precautions.

• Pregnancy: Lassa fever has very high maternal and fetal mortality, especially late in pregnancy (over 80% fetal loss, 30% maternal mortality in the third trimester). Yellow fever vaccine is generally not given in pregnancy (except outbreaks). Japanese encephalitis vaccine is generally deferred (not relevant to these agents). Strategies lean toward mosquito avoidance and individualised counselling. ^[5][7]
• Children: yellow fever vaccine not under 9 months; Rift Valley fever and CCHF affect all ages with no special paediatric antiviral. Filovirus supportive care applies to children; mAb dosing is weight-based.
• Older adults: yellow fever vaccination risk-benefit above 60 years needs care; West Nile (not a VHF) is more severe with age, relevant only for differential. ^[7]
• Immunocompromised: live yellow fever vaccine contraindicated in significant immunosuppression; VHF supportive care and infection control stricter.
• Survivors: structured follow-up after Ebola/Marburg; long-term sequelae after hantavirus and Rift Valley fever (meningoencephalitis).

These infections are managed where tests and intensive care are scarce more often than where they are not. What matters is what can be done with observation and fluids.

• Recognise early: any febrile patient from an endemic area, or with animal/tick/mosquito exposure, could have a VHF. Look for vascular leak, thrombocytopenia and organ dysfunction rather than wait for tests.
• Fluids: oral rehydration where the patient can drink; IV balanced crystalloids (Ringer's lactate) where not. Avoid saline-heavy resuscitation where possible. Track haematocrit and platelets if available; otherwise urine output and perfusion.
• Antibiotics: presumptive broad-spectrum antibiotics only where bacterial sepsis or co-infection suspected; avoid routine antibiotics in low-likelihood patients.
• Tranexamic acid: not recommended for haemorrhage in filovirus disease (except postpartum haemorrhage).^[1]
• Ribavirin: uncertain benefit in Lassa and CCHF, dosing unsettled; use only in trials if possible. For HFRS, IV ribavirin early can help; for HPS there is no specific therapy.
• Isolation: single room, standard plus contact precautions, hand hygiene, PPE by risk. HCID-level PPE for suspected Ebola/Marburg/Lassa/CCHF. Even without fancy rooms, segregate and restrict visitors, use dedicated equipment, and terminal decontamination.
• Community and animal measures: rodent control, safe food storage and cooking; tick control on animals before slaughter; mosquito control (nets, repellents, clearing breeding sites); livestock vaccination for Rift Valley fever before outbreaks.
• Referral: confirmed or strongly suspected Ebola/Marburg/Lassa/CCHF should go to the designated HCID treatment centre (in the UK, the HLIU) wherever possible, but good supportive care at the first facility saves lives while transfer is arranged.

The UK acute-hospital pathway (risk assessment, malaria screen, Imported Fever Service testing, HLIU transfer) is set out as a flow in the isolation section. Use it together with the disease comparison table above.

• Viral haemorrhagic fever is a syndrome of several enveloped RNA viruses: arenaviruses (Lassa), filoviruses (Ebola, Marburg), bunyaviruses (Crimean-Congo haemorrhagic fever, Rift Valley fever, hantaviruses) and flaviviruses (yellow fever, dengue).
• Ebola, Marburg, Lassa and Crimean-Congo haemorrhagic fever are high consequence infectious diseases in the UK because they pass person to person; yellow fever, Rift Valley fever, hantavirus and the others are not.
• The unifying pathology is endothelial injury and vascular leak; bleeding is common but not the usual cause of death; shock, fluid loss and organ failure are.
• Every acutely unwell patient with feverishness and a relevant travel or exposure history within 21 days should be risk-assessed for VHF before a benign diagnosis is accepted, with malaria screened first. ^[3]
• Ebola and Marburg: profuse diarrhoea and vomiting with massive fluid loss; rash around day 5; late haemorrhage in a minority; viral RNA in semen for months. Treatment is optimised supportive care plus monoclonal antibody (mAb114 50 mg per kg or REGN-EB3 150 mg per kg as a single infusion) when it is Zaire ebolavirus.
• Lassa: about 80% mild; severe disease with facial swelling, bleeding, hypotension; hearing loss in up to 25% of survivors; very lethal in pregnancy. Ribavirin uncertain.
• Crimean-Congo haemorrhagic fever: tick or tissue exposure; abrupt systemic illness with hepatitis; about 30% fatality. Ribavirin off-label with uncertain dosing.
• Yellow fever: two phases, jaundice and bleeding in severe cases; about half of severe cases die. No specific antiviral; vaccine single dose, lifelong.
• Hantavirus splits by organ: HPS (lungs, about 38% fatality, deaths 24 to 48 hours after onset) versus HFRS (kidneys, 5 to 15% in Hantaan/Dobrava, under 1% in milder forms); intravenous ribavirin early helps HFRS.
• Rift Valley fever: usually mild; three severe forms (ocular, meningoencephalitis, haemorrhagic about 50% fatality); no licensed human vaccine.
• Supportive care for filoviruses: balanced crystalloids (Ringer's lactate), protocolised oral/IV fluids, lactate and capillary refill to guide resuscitation, early norepinephrine for shock, presumptive antibiotics only for suspected sepsis, tranexamic acid only for postpartum haemorrhage (not routine haemorrhage).
• In the UK: minimal/at risk/confirmed pathway; single side room; HCID PPE for at risk and confirmed; HLIU for confirmed; VHF testing by the Imported Fever Service (6 to 8 hours); contact monitoring for 21 days; airborne transmission not supported epidemiologically, but precautions for aerosol-generating procedures.
• Prevention: infection control, PPE, isolation, contact tracing; vector and rodent control; vaccination where available (yellow fever, animal vaccination for Rift Valley fever); no population screening, just a good travel/exposure history.

Plain text: malaria; mosquito-borne viral infections (cross-check yellow fever); sepsis; meningococcal septicaemia; typhoid and enteric fever; leptospirosis; brucellosis; plague; Q fever; renal failure; acute respiratory distress syndrome; pregnancy in infectious disease; infection prevention and control; travel medicine. (These are listed as plain text; TopicLink-style links are not used here.)