Rabies and animal bites

• Rabies is a viral infection of the brain and spinal cord, almost always spread by the saliva of an infected mammal through a bite or scratch that breaks skin or mucosa, and it is 100% fatal once clinical symptoms appear.^[2]
• Among the roughly 44,203 human rabies deaths estimated each year, about 99% are dog-mediated and about 40% occur in children under 15 years of age.^[2]
• Post-exposure prophylaxis (PEP) prevents rabies in almost all cases if it is started promptly: immediate washing of the wound for at least 15 minutes, a course of rabies vaccine, and rabies immunoglobulin or monoclonal antibodies for severe exposures.^[2]
• PEP regimens differ depending on whether the person was previously immunised. People who have never been vaccinated against rabies receive human rabies immunoglobulin (HRIG) at 20 IU per kg plus vaccine on days 0, 3, 7 and 14 (with a fifth dose on day 28 if they are immunocompromised).^[1]
• Most animal bites do not transmit rabies. Bite wounds most often become infected with the polymicrobial oral flora of the biting animal, especially Pasteurella species (recovered from about half of infected dog bites and three-quarters of infected cat bites) and, after dog bites, Capnocytophaga canimorsus in a minority, sometimes fulminant, of cases.^[5][6]

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

1. State what rabies is, how it is transmitted, and what its incubation period and clinical forms are.
2. Classify an animal exposure into the three WHO categories and know which exposures require PEP.
3. Explain why immediate wound washing matters and describe correct technique.
4. Prescribe PEP correctly for a person who has never been vaccinated, for a previously vaccinated person, and for someone who is immunocompromised.
5. Manage rabies risk where the biting animal can be observed, and state when no further treatment is needed.
6. Recognise a high-risk bite wound and choose antibiotics, dose, route and duration for Pasteurella and other bite flora.
7. Describe the presentation, risk factors and treatment of Capnocytophaga canimorsus sepsis.
8. Explain the rabies diagnostic possibilities before and after symptoms and the role of palliative care.

A useful set of distinctions:

• Rabies disease is the clinical, fatal encephalitis. Rabies exposure is any contact that could have inoculated virus; only a minority of exposures lead to disease if PEP is given promptly.
• Dog-mediated rabies accounts for around 99% of human cases, and dog vaccination is therefore the principal prevention strategy. In some regions, other mammals such as bats, foxes, raccoons and skunks are important reservoirs.^[2]
• Although the classical picture is a furious, hydrophobic encephalitis, a paralytic form accounts for roughly one in five cases and is frequently mistaken for Guillain-Barre syndrome, poliomyelitis or another cause of paralysis.^[2]

Rabies virus (RABV) is the type species of the genus Lyssavirus. It enters through a skin or mucosal breach, binds to receptors at the nerve ending, and travels by retrograde axonal transport to the brain and spinal cord. The incubation period depends on the site of entry (its distance from the brain), the severity of the exposure, the viral inoculum and the host's age and vaccination status.^[3]

A species pattern:

• Globally, dogs (including puppies) are the source in 99% of human cases.^[2]
• In the Americas, where dog-mediated rabies is largely controlled, haematophagous (blood-feeding) bats have become the main source of human rabies. Bites from rodents are not known to transmit rabies, and human-to-human transmission through bites or saliva has never been confirmed, although it is theoretically possible.^[2]
• In the United States, most human cases are associated with rabid bats rather than dogs or cats. Rabies in domestic cats and dogs is rare there; 2008 United States surveillance found rabies in about 4.3% of tested cats and 1.1% of tested dogs, and canine rabies virus variant transmission among dogs was eliminated in 2004.^[5]

Epidemiology:

• Worldwide, newer Global Health Estimates attribute about 44,203 annual deaths to rabies, with substantial under-reporting because of weak surveillance, under-diagnosis and misdiagnosis.^[2]
• About 40% of deaths are in children under 15, who are also more likely to have their exposure unreported and to have shorter incubation periods.^[2][3]
• More than 29 million people receive human rabies vaccine each year, and the cost of rabies post-exposure prophylaxis (including travel and lost income) remains a heavy burden for families earning one or two dollars a day.^[2]
• Rabies is present on every continent except Antarctica, and three countries (Bhutan, Chile and Mexico) have been validated by WHO for elimination of dog-mediated human rabies as a public health problem.^[2]

After inoculation, rabies virus first replicates in muscle or connective tissue at the exposure site and then binds to receptors at the neuromuscular junction or at sensory nerve endings (notably the nicotinic acetylcholine receptor and other neural cell adhesion molecules). Transport proceeds by retrograde axonal flow along peripheral and cranial nerves, which is why the incubation period is shorter for exposures on the face, neck or hands than for exposures on the trunk or legs, and why extensive initial wound washing can strip away virus before this step begins.^[2]

Once the virus reaches the central nervous system it multiplies massively in neurones. Only after central amplification does the virus travel outward again to the salivary glands, the eyes, skin, heart, gastrointestinal tract and other organs. This explains the combination of salivary infectivity, hydrophobia from brainstem involvement, and occasional myocarditis and acute respiratory distress in advanced disease. Because the incubation period proceeds outside the bloodstream and behind the blood-brain barrier, neither antibodies in serum nor standard antivirals are reliably effective once symptoms have started, and there is no WHO-approved test for pre-symptomatic infection.^[2]

The incubation period is typically 2 to 3 months, although it may range from as short as one week to more than one year, depending on the location of virus entry and the viral load. Children may have shortened incubation periods.^[2][3]

The first symptoms last for several days and are often nonspecific: fever, pain, fatigue and headache. A characteristic and highly suggestive finding is discomfort, prickling or an itching sensation at the site of the bite, which reflects viral replication in local nerve roots. After this prodrome, progression to severe neurological disease occurs within about two weeks.^[3]

• Furious rabies is the more common form. It produces episodes of hyperactivity, agitation, hallucinations and disorientation interspersed with apparently lucid intervals, together with hypersalivation, cranial nerve palsies, hydrophobia (an involuntary, painful spasm of swallowing triggered by the sight or sound of water) and aerophobia (the corresponding response to drafts or fresh air). Death occurs within a few days from cardiorespiratory arrest.^[2]
• Paralytic rabies accounts for about 20% of cases. Weakness begins at the wound site and spreads to a symmetrical, ascending paralysis that mimics Guillain-Barre syndrome, with fever, sphincter disturbance and respiratory muscle weakness. The course is longer and quieter, which makes it easy to miss and contributes to under-reporting.^[2]

All patients with rabies present with encephalitis. The disease is virtually 100% fatal once symptoms appear, and only exceptionally rare survivors have been reported, usually with severe residual neurological deficit. Positive indicators that favour rabies include a nonspecific prodromal phase, neurologic signs consistent with encephalitis or myelitis, dysphagia, hydrophobia, paresis and autonomic instability, and progression of neurological signs. Negative indicators include improvement or lack of change after weeks of illness and survival beyond four weeks.^[2][3]

Once symptoms have appeared, management is supportive and palliative: airway protection, sedation, control of spasms and fear, and compassionate care for the patient and family. There are no effective antiviral or immunological curative treatments at this stage.^[2]

Rabies should be considered in any patient with unexplained encephalitis, especially when there is a history of animal contact (including unremembered bat exposure), and the public health department should be consulted immediately to arrange testing. In the United States, confirmatory testing is on clinical specimens (skin biopsy, saliva, cerebrospinal fluid and serum) coordinated by public health laboratories; the biting animal, if available, should be tested.^[2][3]

Exposure risk assessment is the most important clinical step, because PEP is given only for categories II and III. Categories (WHO definitions, used in almost all international and national guidance):

Both Category II and Category III exposures require human rabies vaccination. Category I exposures do not.^[2]

Atypical exposures that still need careful judgement include unprovoked exposures to wild animals, bites from animals known to be rabid or suspected to be, deep head and neck bites, exposure of a child, the immunocompromised, or exposures in people who are already ill. Aerosol transmission, transmission by raw meat or milk and organ-transplant transmission are all extremely rare but have been reported.^[2]

Ask what happened, the species and availability of the animal, whether the bite was provoked, the behaviour of the animal then and later, the timing of its last rabies vaccination if a pet, and the patient's tetanus and rabies vaccination status. Was the wound washed at the time? Are there smaller scratches or licks that everyone forgot? Bat exposures in particular are often trivial and unnoticed.

For dogs, cats and domestic ferrets that are healthy, available and can be observed, a widely used rule is that if the animal remains well through a 10-day period after the bite, rabies is very unlikely and PEP can be stopped. For other species the infectious period is less well characterised, so clinical management and any observation or testing should be agreed with the local health department. Bites to the head and neck, deep or multiple wounds, immunocompromise, and exposure to a bat, wild mammal or unprovoked animal warrant more conservative management. These details should be agreed with the local public health veterinarian or health department. (These management rules come from standard public health practice rather than the cited primary sources and should be checked against local guidance before use.)

Immediate, thorough cleansing of all wounds, scratches and mucosal exposures with water and soap for at least 15 minutes is recommended, followed where possible by an antiseptic or virucidal preparation such as povidone-iodine. In animal experiments, thorough cleansing alone markedly reduced the likelihood of rabies, even without vaccine. Decisions about primary closure, antibiotics and tetanus status should be made with the patient and the wound.

Start PEP as soon as possible after the exposure. It is effective even when begun days or weeks later, but it should never be delayed while waiting for confirmation of rabies in an animal. Exposures treated outside the United States with a regimen recognised by WHO generally need no further treatment; if a regimen was not WHO-recognised or was not completed, further doses or antibody testing may be required.^[1]

Wound washing, active immunisation and (for Category III in unimmunised people) passive immunisation are the three parts of PEP.

Practical details, all of which carry the authority of the ACIP-based CDC guidance (last reviewed September 2026):

• HRIG provides immediate neutralising antibody until the vaccine produces its own response. It is given only once, on day 0. Do not give more than the recommended dose: if a small wound on a finger is not sufficiently infiltrated, it may be re-infiltrated up to a total of 40 IU/kg. A higher total than this can blunt the antibody response.^[1]
• HRIG should never be administered in the same syringe or at the same site as the first vaccine dose, but subsequent vaccine doses may be given in the same site where HRIG was given. If both were given in the same site by error, repeat the vaccine in a distant site and consider re-giving HRIG up to 40 IU/kg total.^[1]
• If HRIG was omitted on day 0, it may still be given up to and including day 7. HRIG is required even when there is no obvious exposure wound, given at a site distant from the vaccination site.^[1]
• Subsequent doses may be delayed by a few days without serious consequence, but lapses of weeks or more require public health consultation. Use the CDC PEP calculator to recover a deviated schedule.^[1]
• Pregnancy is not a contraindication, PEP is suitable for all ages including infants, and no rabies vaccine is known to be contraindicated.^[1]

People who received a complete pre-exposure course or a full course of PEP in the past, or an acceptable alternative, do not need HRIG. Their immune memory allows an anamnestic response to two doses.^[1]

• Vaccine (HDCV or PCECV) 1.0 mL intramuscularly in the deltoid (anterolateral thigh in children), not in the gluteal area, given on days 0 and 3 only.
• No HRIG.
• At the same time give thorough wound care as for any patient.

Pre-exposure prophylaxis (PrEP) is for people at high risk of rabies: laboratory workers handling live rabies virus, animal disease control staff, wildlife rangers, people living in remote rabies-endemic areas with poor access to biologics and, in some circumstances, travellers.^[2] In the United States, ACIP now recommends a two-dose primary series on days 0 and 7 instead of the former three-dose series, with a one-time titer or booster between 1 and 3 years (or between 3 weeks and 3 years, depending on risk category) and risk categories redefined into five groups; immunocompromised patients and those who did not respond should be tested for rabies virus neutralising antibody, with a sufficient level taken as 0.5 IU per mL.^[8] People who have received ACIP-recommended PrEP require only two doses of vaccine (days 0 and 3) and no immunoglobulin after any subsequent exposure.^[1]

Intradermal delivery reduces the amount of vaccine used and the cost without compromising safety or efficacy, and these route-specific details should be checked against current national guidance before practice. ^[2]

If the medical history suggests a poor response to vaccination (immune compromise, immunosuppression, severe malnutrition, major intercurrent illness), PEP should use a five-dose regimen: HRIG on day 0 plus vaccine on days 0, 3, 7, 14 and 28. Avoid immunosuppressive agents during PEP unless essential, and consult about delaying them. After the series, test for rabies virus neutralising antibody; patients who fail to mount a response should be managed with state or CDC rabies experts, who may advise reassessment of risk, further doses or off-label routes of administration. CDC's National Rabies Reference Laboratory can perform serologic testing, accessed through the state health department. The same 0.5 IU per mL threshold is used to judge an adequate response. ^[1]

Most bite wounds heal uneventfully, but infection is more likely after cat bites, puncture wounds, hand wounds, bites in older or immunocompromised people and bites not promptly cleaned. NICE NG184 provides a practical framework: everyone with a bite should have the type and severity assessed (including animal, site, depth and whether infection is present), an antibiotic is offered if there are symptoms or signs of infection (increased pain, inflammation, fever, discharge or an unpleasant smell), and prophylaxis is considered when the bite is high risk.^[4]

Pasteurella species are Gram-negative coccobacilli that form part of the normal oral flora of dogs, cats and many other animals. They are isolated from infections after about 50% of dog bites and about 75% of cat bites.^[5] In the prospective Emergency Medicine Animal Bite Infection Study Group series of 50 infected dog bite wounds, Pasteurella was the commonest aerobic genus in 50% of wounds, with Pasteurella canis in 26%, Pasteurella multocida subspecies multocida in 12%, Pasteurella stomatis in 12%, Pasteurella multocida subspecies septica in 10%, Pasteurella dagmatis in 4% and Pasteurella multocida subspecies gallicida in 2%. In 57 infected cat bite wounds, Pasteurella accounted for 75% of isolations, with Pasteurella multocida subspecies multocida in 54% and Pasteurella multocida subspecies septica in 28%, followed by Pasteurella dagmatis in 7%, Pasteurella stomatis in 4% and Pasteurella canis in 2%.^[5]

Clinical points:

• Bite wounds are usually polymicrobial. An infected dog or cat bite typically grows 2 to 5 bacterial species, mixing aerobes (Pasteurella, Streptococcus, Staphylococcus) and anaerobes such as Fusobacterium and Porphyromonas.^[5]
• Pasteurella infection declares itself quickly: the median time from cat bite to first symptoms is about 12 hours and from dog bite about 24 hours.^[5]
• Pasteurella multocida subspecies multocida and subspecies septica are associated with more serious systemic infection, and subspecies septica has a particular tendency to cause nervous system infections such as meningitis. Septic arthritis, osteomyelitis, tendon sheath infection and bloodstream infection can follow, especially in older adults.^[5]
• Pasteurella organisms are generally not susceptible to erythromycin, lincosamides such as clindamycin used alone, dicloxacillin or cephalexin, so these are not recommended as single agents for animal bites. Amoxicillin with clavulanate, doxycycline plus metronidazole in penicillin-allergic patients, or clindamycin plus a fluoroquinolone are the recommended alternatives.^[5]

Capnocytophaga canimorsus is a fastidious Gram-negative rod of the oral flora of healthy dogs and cats, transmitted principally by dog bites. It can produce a localised wound infection but is more feared for invasive infection, particularly in people who have had a splenectomy or have liver disease or alcohol use disorder. In a systematic review of all reported cases, an estimated 484 patients were described, with a median age of 55 years, two-thirds male, a case-fatality rate of about 26%, and preceding dog bites in 60% of cases (in a further 27% there had been scratches, licking or other contact with a dog or cat).^[6] The organism possesses virulence factors including catalase and sialidase production, gliding motility, cytotoxin production and resistance to killing by complement, which help explain why it can become established before symptoms appear.^[6]

Presentation of invasive disease:

• Severe sepsis and septic shock, often within days of the exposure; patients with meningitis tend to have longer incubation periods than those with sepsis.
• High-grade bacteraemia, purpura fulminans, symmetrical peripheral gangrene and disseminated intravascular coagulation.
• Meningitis (older patients, more men, lower mortality than in sepsis), endocarditis and eye infection.
• Predisposition is marked: prior splenectomy in 59 of the reviewed patients, alcoholism in 58.^[6]

Diagnostic clues: the organism grows slowly, with a mean of about 6 days and a range of 1 to 14 days in blood culture, improved by culture in a carbon dioxide-enriched atmosphere on horse blood or chocolate agar; MacConkey and triple-sugar-iron agars do not support growth. Examination of Gram-stained buffy coat smears or of material from petechial lesions can give an early diagnosis, while ordinary swabs are often negative. Patients with prior splenectomy present more frequently with high-grade bacteraemia than those with intact spleens.^[5][6]

Treatment is with a high-dose beta-lactam; penicillin is the drug of choice, although many clinicians use a third-generation cephalosporin or a beta-lactamase inhibitor combination, and carbapenems are increasingly favoured if beta-lactamase-producing strains are suspected. Susceptible strains should be reassessed as cultures return. Early wound care and prophylactic antibiotics after dog or cat bites in immunocompromised, asplenic or heavy-drinking patients are appropriate, and these patients should be warned to seek care early if a bite becomes painful, red or feverish.

Rabies:

• Encephalitis with hydrophobia and aerophobia, coma and death in almost every case once symptoms appear.^[2]
• Paralytic rabies with ascending weakness and respiratory failure.
• Myocarditis and acute respiratory distress in advanced infection.
• Organ transplant transmission and, very rarely, aerosol or raw-meat transmission have been described.^[2]

Bite infections and other complications of an animal bite:

• Soft-tissue infection, cellulitis, abscess, tenosynovitis, septic arthritis and osteomyelitis, particularly of the hand.
• Capnocytophaga or Pasteurella sepsis with purpura fulminans and disseminated intravascular coagulation, most often in asplenic and immunocompromised patients.^[6]
• Nerve or tendon laceration, fracture, dislocation and vascular injury from the mechanical force of the bite, especially in children.^[1]
• Rabies exposure requiring prolonged PEP.
• Tetanus, if immunisation is inadequate (review tetanus status for every significant bite and give vaccine or immunoglobulin per national guidance).
• Psychological consequences, including fear of animals and post-traumatic distress, are common and often overlooked.

Human rabies, once symptomatic, is almost uniformly fatal, usually within days for the furious form and within a few weeks for the paralytic form; only rare survivors have been reported and they usually have severe neurological impairment. By contrast, PEP given in time is almost completely protective, provided that the wound is properly washed and that the correct schedule and, for unimmunised people, immunoglobulin are given. The combination of wound care and vaccine is the principle behind the global Zero-by-30 strategy, even where immunoglobulin is scarce, because washing alone has a substantial effect.

For bite infections, prognosis is generally excellent with appropriate antibiotics and, where necessary, surgical debridement or joint washout. Capnocytophaga sepsis is an exception, with a case-fatality rate of about one in four and a high rate of amputation in survivors of purpura fulminans.^[6] Pasteurella osteoarticular and deep hand infections can leave long-term stiffness and functional loss despite adequate treatment.

Prevention is layered:

• Mass dog vaccination is the single most effective preventive measure, because dogs are the source of 99% of human cases. Public education on dog behaviour and bite prevention, especially for children, and responsible pet ownership are its essential extensions.
• Safe, prompt and affordable access to PEP for every exposed person, supported by intradermal delivery that reduces cost by 60 to 80% without loss of safety or efficacy. ^[2]
• Cross-sectoral One Health cooperation between human and veterinary services, including reporting and follow-up of biting animals.
• As of September 2026, three countries have been validated for elimination of dog-mediated human rabies, and many European countries are self-declared free of infection in dogs in compliance with the WOAH terrestrial code.^[2]

Before symptoms appear there is no screening test for rabies, so exposure risk assessment is the screening step that matters. Where a person is repeatedly exposed, documenting and monitoring response to vaccine may be worthwhile. In endemic areas, animal rabies surveillance and animal vaccination programmes provide the population-level screen.

Children. Children bear about 40% of rabies deaths, are more likely to be bitten on the face and neck (with shorter incubation), less likely to report a bite, and often have smaller, hair-covered wounds. Wound washing must be parent-supervised and thorough; exposure risk assessment should be thorough even for apparently trivial bat contacts. Pre-exposure vaccination is not routine except for high-risk groups, but the two-dose schedule makes it more feasible where indicated. Pasteurella and Capnocytophaga infections after a bite follow the same patterns as in adults; weight-based antibiotic dosing is used. Children are particularly at risk of tendon injury from a bite and should be assessed for function.

Pregnancy and breastfeeding. Neither rabies PEP nor bite prophylaxis is contraindicated in pregnancy; untreated rabies in the mother would be fatal, and vaccine and immunoglobulin are safe. Where co-amoxiclav is unsuitable in a pregnant patient with penicillin allergy, NICE recommends specialist advice.^[4]

Immunocompromised and asplenic patients. These patients need the five-dose PEP schedule with HRIG, antibody follow-up, and a low threshold for prophylactic antibiotics after a bite because Capnocytophaga can be lethal in them. They are also more likely to mount a poor vaccine response and should be advised that their risk of rabies after exposure is higher unless PEP is completed perfectly.

Older adults. Frailty, anticoagulant use and poorer wound healing complicate bite management; deep hand infections and tendon involvement are more dangerous, and systemic infection can precipitate frailty and delirium.

• Diagnosis of rabies exposure is clinical and does not need a laboratory early on. Risk assessment, category classification, washing for 15 minutes and prompt PEP are all low-tech.
• Wound washing with soap and clean water for at least 15 minutes is available everywhere. ^[2]
• RIG scarcity is the main access problem. Where human rabies immunoglobulin is unavailable, WHO supports rabies monoclonal antibodies as an alternative, and equine rabies immunoglobulin is effective where it is available. Intradermal vaccine delivery cuts the amount of vaccine used by 60 to 80% and reduces vial use.
• PEP outside the clinic may be started with local emergency care and rapid referral. WHO recommendations are that any WHO-recognised regimen is acceptable, so local practice should be compared with WHO schedules before judging it inadequate.
• Animal observation and culling: culling free-roaming dogs is not effective in controlling rabies; mass vaccination of dogs is the effective strategy. Do not delay human PEP while arranging animal testing.
• Bite infection care can be delivered with oral co-amoxiclav where possible, surgical cleaning and debridement of deep hand wounds, and referral when bone, joint or tendon is involved. For patients who cannot take penicillin, doxycycline plus metronidazole (adults) or co-trimoxazole in children under 12 are the NICE alternatives.^[4]

Rabies as an encephalitis and clinical neurology; viral trafficking along peripheral nerves; tetanus prophylaxis after wounds; animal bite wound assessment and soft-tissue infections; sepsis recognition and management; asplenia and overwhelming infection; vaccine immunology and memory; global health and neglected tropical diseases.