Leptospirosis

What it is

Leptospirosis is caused by spirochaetes of the genus Leptospira, mainly L. interrogans, L. kirschneri and L. borgpetersenii. There are hundreds of serovars, grouped into serogroups. Each serovar has maintenance hosts, which become chronically infected, rarely become ill and shed leptospires in urine for months or years (for example, the rat for Icterohaemorrhagiae, the dog for Canicola or cattle for Hardjo), and incidental hosts, in which infection is usually more severe.

The bacterium is transmitted by direct contact with the urine of a carrier or, more often, indirectly through contaminated water, mud or soil, where it survives well in warm, moist conditions; this is why cases increase after heavy rain and flooding. It enters through mucous membranes or through skin that is damaged or softened by water. After a phase of leptospiraemia it spreads through the body, damages the vascular endothelium and colonises mainly the kidneys and liver. Animals that survive can remain renal carriers.

It is a zoonosis: people are infected by contact with animal urine or contaminated water, and human disease ranges from a flu-like illness to severe forms with kidney failure, jaundice and pulmonary haemorrhage. It is notifiable in many countries.

Who it affects

Dogs of any age, breed and environment. Risk increases with access to stagnant water, rivers and ponds, contact with rodents, wildlife or livestock, and rainy seasons. According to the 2023 ACVIM consensus, it also affects small-breed dogs in urban areas, puppies as young as 11 weeks, geriatric dogs and incompletely vaccinated dogs. In cats infection is possible, but clinical disease is described infrequently.

Anatomy involved

• Kidneys: leptospires colonise the renal tubules and cause tubulointerstitial nephritis with acute kidney injury, which may be polyuric or oliguric to anuric. From the tubules they are shed in urine. On ultrasound the kidneys may appear enlarged, with perirenal fluid and pelvic dilation.
• Liver: hepatocellular damage and cholestasis, with increased liver enzymes, hyperbilirubinaemia and jaundice. Some serovars cause more marked liver disease than others.
• Lungs: leptospiral pulmonary haemorrhage syndrome (LPHS) results from damage to the endothelium of the pulmonary capillaries and causes diffuse alveolar haemorrhage. It produces tachypnoea, dyspnoea and sometimes haemoptysis, a caudodorsal interstitial to alveolar pattern on radiographs, and greatly worsens the prognosis.

Clinical signs

Many infections are subclinical. In the acute form there is lethargy, anorexia, vomiting, fever, abdominal or muscle pain, stiffness and reluctance to move, polyuria and polydipsia or, conversely, oliguria or anuria, jaundice and a bleeding tendency (petechiae, epistaxis, melaena) from thrombocytopenia or disseminated intravascular coagulation. Other signs are uveitis, tachypnoea and dyspnoea from lung involvement. Some dogs show only polyuria and polydipsia or hepatitis.

Diagnosis

• Laboratory tests: azotaemia, increased liver enzymes and bilirubin, thrombocytopenia, neutrophilic leucocytosis and electrolyte disturbances. In urine, low specific gravity, glucosuria without hyperglycaemia, proteinuria and casts.
• Microscopic agglutination test (MAT): the reference serological test. The most reliable approach is to compare an acute-phase titre with a convalescent one, 1–2 weeks later; a fourfold or greater rise confirms infection. A single high titre is suggestive, but vaccine antibodies and previous exposure cause titres and, in the first week, the result can be negative. There is large variation between laboratories and the MAT does not reliably identify the infecting serogroup.
• PCR: detects the bacterium in blood early in the disease and in urine somewhat later; testing both samples is recommended, before antibiotics are given and together with serology. A negative PCR does not rule out the disease.
• Rapid in-clinic antibody tests help decision-making, but are confirmed with MAT or PCR.
• Imaging: abdominal ultrasound and thoracic radiographs to assess the kidneys, liver and lungs.

Treatment and prevention

Antibiotics are started as soon as the disease is suspected, without waiting for results. Treatment usually starts with a parenteral penicillin derivative if the dog is vomiting, followed by doxycycline, which also eliminates the renal carrier state; if the dog tolerates it orally, it can be used from the start. Supportive treatment includes fluid therapy adjusted to urine output (taking care not to overhydrate oliguric dogs), antiemetics, gastroprotectants and nutrition. Dogs with oliguric or anuric acute kidney injury that does not respond benefit from haemodialysis, and those with severe pulmonary haemorrhage may need oxygen or mechanical ventilation.

Sick dogs and their urine are handled as infectious material: gloves, isolation and disinfection of surfaces. Vaccination protects only against the serogroups included in the vaccine and is repeated every year. Classic guidelines consider it non-core, but recommended for dogs at risk of exposure, which today includes many urban dogs. Rodent control and keeping dogs from drinking or swimming in stagnant water also help.

In cattle

In cattle the most important serovar is Hardjo (L. borgpetersenii serovar Hardjo type hardjobovis and L. interrogans serovar Hardjo type hardjoprajitno). Cattle are its maintenance host: infection persists in the kidneys and genital tract, is transmitted in urine, venereally and across the placenta, and most infected cows show no signs outside pregnancy and lactation. Sheep also maintain Hardjo. Other serovars, such as Pomona or Icterohaemorrhagiae, infect cattle incidentally and cause more severe acute disease.

• Kidneys: the renal tubules harbour leptospires for a long time and the cow sheds them in urine, the main source of infection for other animals and for people. In calves an interstitial nephritis with whitish foci in the renal cortex may be seen.
• Uterus: infection of the placenta and fetus causes abortion, usually in the last third of gestation and weeks after infection, stillbirths and weak calves. Persistent infection of the genital tract is associated with infertility: more services per conception and more days to conception.
• Udder: in the acute phase, Hardjo causes milk drop syndrome ("agalactia"): a sudden fall in yield in all four quarters, which become flaccid, with thick, yellowish or colostrum-like milk, without the signs of inflammation of mastitis, often with transient fever and in several cows of the herd at once.

In calves, incidental serovars cause fever, haemolytic anaemia, haemoglobinuria and jaundice, sometimes fatal. Diagnosis is made at herd level: serology (MAT or ELISA, also on bulk-tank milk), PCR on urine and examination of aborted fetuses (PCR or fluorescent antibody testing on fetal kidney). In Hardjo abortions the dam's titre may be low. Control relies on herd vaccination with vaccines that include Hardjo, antibiotic treatment of carriers, quarantine and treatment or vaccination of purchased animals, rodent control, and avoiding shared grazing with sheep and access to contaminated water. Antibiotic use in food-producing animals is subject to each country's regulations and their withdrawal periods for milk and meat.

It is an occupational zoonosis: farmers, milkers (from urine splashes in the milking parlour), veterinarians and abattoir workers are the most exposed. Herd vaccination, hygiene measures and protective equipment reduce the risk.

In the horse

In horses exposure is very common and most infections cause no signs. Serovar Bratislava is the one most often found in serological studies and is considered horse-adapted, but it has not been shown to cause clinical disease in North America, where most clinical cases are due to Pomona type kennewicki; the serovars involved vary by region. Clinical disease mainly affects three organs:

• Eyes: leptospires can remain inside the eye and trigger, months or years after infection, equine recurrent uveitis, the leading cause of blindness in the horse. Antibodies produced inside the eye, bacterial DNA and even live leptospires are found in the aqueous humour and vitreous of many affected eyes. Systemic antibiotics do not clear the intraocular infection; in Europe vitrectomy is used in eyes with proven leptospires.
• Uterus: infection of the placenta and fetus causes abortion, mainly in the second half of gestation, stillbirths and weak or sick newborn foals; a healthy foal with antibodies may also be born. The mare usually shows no other signs at the time of abortion, but may shed leptospires in urine for weeks. The placenta shows placentitis and the fetus lesions in the liver and kidneys.
• Kidneys: in young horses leptospires can cause acute kidney failure, which responds to antibiotics and supportive care. The kidneys are also where the bacterium persists in carriers.

In abortion, diagnosis is made with PCR on the placenta and fetal kidney, fluorescent antibody testing on fetal kidney and MAT on fetal heart blood and the mare's serum; in uveitis, with antibodies and PCR on aqueous humour or vitreous. Antibiotics are used for kidney failure; giving them to exposed pregnant mares to prevent abortion or urinary shedding is practised, but its efficacy is not documented. In North America an equine vaccine against Pomona type kennewicki is licensed. The horse is a food-producing species in many countries: in the EU its passport states whether it is excluded from the food chain, and this determines which medicines may be used and with which withdrawal periods.

Aborted fetuses, the placenta and the mare's urine are a source of infection for the people who handle them.

Key studies

• ACVIM consensus statements (Sykes et al., 2011, updated in 2023): the reference for dogs. The 2010 statement recommends diagnosis with acute and convalescent MAT titres, with or without PCR, warns of large interlaboratory variation in the MAT and that it does not predict the serogroup, and recommends doxycycline to clear the bacterium from the renal tubules and annual vaccination of dogs at risk. The 2023 update, voted on by 12 experts using the Delphi method, incorporates the new diagnostic methods and vaccines and notes that the disease also affects small-breed urban dogs, puppies as young as 11 weeks, geriatric dogs and incompletely vaccinated dogs. These are expert opinions, not studies.
• Bergmann Esteves et al. (2022), systematic review and meta-analysis of 13 challenge trials and 8 observational studies covering 12 canine vaccine brands. Vaccinated dogs had a relative risk of 0.16 of developing disease and 0.12 of becoming renal carriers compared with unvaccinated dogs, an overall protection of 84% and 88%. Protection against Canicola, Australis and Grippotyphosa was inconsistent for some brands, immunity lasted at least one year under experimental conditions and post-vaccination MAT titres did not correlate with protection. Most of the data come from experimental infections.
• Moreira et al. (2025), systematic review and meta-analysis of 77 MAT serology studies in cattle published between 2018 and 2023. The pooled global seroprevalence was 39.5% (95% CI 33.1–46.3%) and 42.7% in the Americas. Hardjo was the most reported serovar (31.1%) and Sejroe the most frequent serogroup (54.9%). Serology does not distinguish infection from vaccination or past exposure.
• Sanhueza et al. (2013), case-control study in New Zealand beef herds comparing cows that aborted with cows that calved normally. Seropositivity to Hardjo was associated with a higher risk of fetal loss (OR 1.84; 95% CI 1.01–3.33), and seropositivity to Pomona in unvaccinated cows with a much higher risk (OR 14.91; 95% CI 1.73–128.84). About 4.7% of fetal losses were attributed to Hardjo and 3.6% to Pomona. It is a serological study in a single country.
• Sanhueza et al. (2018), systematic review and meta-analysis of 9 trials of commercial Hardjo vaccines in cattle. Efficacy in preventing urinary shedding of leptospires was 88.7% (95% CI 81.0–93.2%), with no heterogeneity between studies. The authors conclude it may be enough to reduce disease in cattle and the exposure of people who work with them.
• Plunkett et al. (2013), randomised controlled trial in 1,894 Holstein cows and heifers on one California dairy (986 vaccinated against Hardjo, with oxytetracycline at the first dose, and 908 given placebo). Vaccination did not improve the probability of conception or reduce pregnancy loss or urinary shedding. A similar trial in 1,446 beef cows at 8 locations (Kasimanickam et al., 2007) also found no differences in pregnancy or calving rates. The widespread idea that vaccinating against Hardjo improves herd fertility on its own was not confirmed in these trials, each carried out under specific conditions.
• Concha et al. (2026), systematic review and meta-analysis of 35 cross-sectional MAT serology studies in horses published between 2015 and 2025. The pooled seroprevalence was 47.2% (95% CI 37.6–57.1%), with large differences between continents (71.0% in North America, 27.0% in Europe). Bratislava was the most reported serovar (15.2%) and Australis the most frequent serogroup (20.0%). Serology does not distinguish active infection from past exposure or vaccination.
• Donahue et al. (1995), study of 2264 equine abortions and stillbirths submitted to a Kentucky laboratory over three foaling seasons: 74 (3.3%) were due to leptospires, and in the 45 culture-positive cases the serovar was almost always Pomona type kennewicki. Fluorescent antibody testing of fetal tissues had a sensitivity of 98.7% and MAT on fetal fluids of 81.3%, both with 100% specificity. It is a single breeding region.
• Erol et al. (2015), cross-sectional study of 339 equine fetuses necropsied in Kentucky: 21 abortions (6.19%) were due to leptospires. Real-time PCR detected all 21 cases, MAT 19 and fluorescent antibody testing 18; placenta and fetal kidney gave similar PCR results. The number of positive cases is small and from a single laboratory.
• Dwyer et al. (1995) and Wollanke et al. (2001), the reference studies on uveitis: in 372 horses in the USA, seropositivity to Pomona was associated with uveitis (OR 13.2) and, in horses with uveitis, with blindness (OR 4.4); in 242 horses undergoing vitrectomy in Germany, leptospires were cultured from the vitreous in 52% and from no control eye. Both are observational studies of selected populations (see the equine recurrent uveitis entry).