IN-DEPTH INTERACTIVE: REPRODUCTIVE DISORDERS – PATHOLOGY TO TREATMENT 2. Leptospirosis
Leptospirosis is a zoonotic disease that affects many domestic and wild animals worldwide. Horses are incidental hosts of several leptospiral serovars; only serovar Bratislava is suspected to be maintained in horses.11 Serologic surveys demonstrate that lep- tospiral infection is common in equine populations. However, most leptospiral infections in the horse are subclinical.12 Clinical disease produces symp- toms that include recurrent uveitis, fever, hemoglo- binuria, jaundice, stillbirth, and abortion mainly in the last trimester.11 There are more than 250 se- rovars of Leptospira spp., but equine leptospirosis has been attributed primarily to L. interrogans se- rovar Pomona type Kennewicki in North America and serovars Bratislava, Grippotyphosa, Copenha- geni, Autumnalis, Hebdomadis, Arborea, and Ic- terohaemorrhagiae in other parts of the world.11 Which serovar presents usually depends on the host in a specific area. Leptospiral infection as a cause of equine abortion has been reported as a diagnosis in 3.1% of cases in Hungary and 2.2% to 3.3% in the United States, whereas in Northern Ireland it has been reported in 35% of cases.11,13 In Kentucky, the source of equine infection is thought to come from the wild animal population, including raccoons, skunks, deer, opossum, and cattle and swine. The Leptospira spp. organisms are shed in the infected animal’s urine and con- taminate water and feed, which are the probable sources of infection for the equine population. Environmental conditions with low-lying swampy areas and stagnant water such as ponds produce higher incidences of the disease. Abortion or stillbirth usually occurs from 6 months of gestation to term, with fetal autolysis present as a result of death in advance of delivery. The mare usually displays no premonitory clinical signs before delivery but often has a high antibody titer against one or more leptospiral serovars. The mare is exposed and then becomes infected and bac- teremic. The organism enters the placenta, caus- ing fetal infection with placentitis and funisitis. The gross allantochorion lesions associated with equine leptospirosis consist of nodular cystic allan- toic masses, edema, necrotic areas of chorion, and necrotic mucoid exudates that coat the chorion.14,15 The microscopic lesions in the allantochorion are thrombosis, vasculitis, mixed inflammatory cell in- filtration of the stroma and villi, cystic adenomatous hyperplasia of the allantoic epithelium, villi necro- sis, and calcification.2,15 The gross and microscopic lesions of the umbilical
cord include mild-to-severe edema, focal-to-multiple sacculations filled with fluid, and coating of the sur- face with a fibrinous exudate, without visible in- volvement of the three primary blood vessels.2 A recent report revealed the surface of the umbilical cord diffusely coated by a dense exudate of mostly nondegenerate neutrophils (funisitis) that were
mixed with fibrin. These neutrophils only infil- trated the cord surface and minimally into the Wharton’s jelly.15 Gross pathologic lesions of the fetus or stillborn foal include icterus and generalized petechial and ecchymotic hemorrhages. Livers are enlarged, mottled, and discolored yellow. Edema is evident in the kidney with pale white radiating streaks in the cortex and medulla.2,15 Microscopic changes show lesions in the liver and kidney to be the most severe. Liver lesions consist of hepatocel- lular dissociation, giant cells throughout the paren- chyma, and leukocytic infiltration of the portal triads. The kidneys contain microabscesses with giant cells, dilated tubules, fibrosis, and multifocal areas of nonsuppurative interstitial nephritis.2 Diagnosis can be made by identifying Leptospira
spp. in the allantochorion, umbilical cord, or fetal kidneys by fluorescent antibody tests (FATs), silver staining, or immunohistochemistry.2,15 A recent study indicated that real-time polymerase chain re- action (PCR) is an effective method for diagnosing leptospiral abortion in horses on both placenta and fetal kidney (and liver when available).16 Expo- sure usually occurs 2 to 4 weeks before abortion; therefore, the affected mares have high serological titers. Serology in the mare and fetus is based on enzyme-linked immunosorbent assay and micro- scopic agglutination tests. Positive diagnosis in mares occurs with serum titers of 1:6400.2 De- tecting leptospires using a FAT is the method of choice for diagnosing leptospirosis in the kidney of aborted fetuses, although immunohistochemistry has shown to have a 78% sensitivity and 100% spec- ificity when compared to the gold standard method of culture.2 Culture, however, is not practical be- cause it takes 6 months for Leptospira spp. to grow. Once an abortion has occurred and leptospirosis is suspected, the mare should be isolated so infective urine and uterine fluids will not expose other mares to the pathogen. Mares that have been pastured with the aborted mare should have Leptospira spp. titers drawn to try to identify potentially exposed mares so treatment can be initiated and abortion hopefully prevented. Serial serum titers may bet- ter identify exposed mares. Sources of infection such as wildlife (skunks for Kennewicki and rac- coons for Grippotyphosa), water, and contaminated feed should be identified so further exposure does not occur. Treatment is successful with 5 mg/kg oxytetracycline intravenously once a day, doxycy- cline 10 mg/kg orally twice a day, and 20 000 IU/kg penicillin G procaine intramuscularly twice daily for 7 to 10 days. Leptospira spp. titers remain high for long periods
of time. In addition, naturally infected mares shed high numbers of nonhost-adapted leptospires in urine for up to 14 weeks; therefore, mares should not be reintroduced to other mares until shedding has ceased and a FAT, silver stain, or PCR shows that the mare’s urine is negative.216 To collect the urine, furosemide must be administered, and then
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