Bacterial Diseases

Leptospirosis

Leptospirosis is a contagious, zoonotic disease caused by numerous serovars of spirochetes in the genus Leptospira. Goats and sheep are less susceptible to leptospirosis than cat­tle, swine, dogs, and humans, and the disease is uncommon in small ruminants.

Etiology

Numerous Leptospira serovars have been identified in clinical caprine leptospirosis, most notably Pomona, Grippotyphosa, Icterohemorrhagiae, and Serjoe. Additional serovars identified infrequently in apparently healthy goats on serologic survey include Autumnalis, Australis, Balcanica, Ballum, Bataviae, Bratislava, Canicola, Hardjo, Hyos, Panama, Pyrogenes, and Wolfii, among others.

Epidemiology

Leptospiral infection of goats is more likely to occur in tropical regions than temperate regions and leptospirosis in small ruminants in tropical regions has been reviewed (Martins and Lilenbaum 2014). Nevertheless, infection has been reported from a wide range of agroclimatic zones in Argentina, Brazil, Israel, Iran, India, Morocco, Kenya, Nigeria, Senegal, Tanzania, Turkey, Spain, Italy, Portugal, the former USSR, Jamaica, Grenada, New Zealand, Mexico, and the United States.

Serious outbreaks of disease with high morbidity and mortality rates in goats have been reported from Iran and Israel. In both countries, serovar Grippotyphosa was involved. In the Iranian epizootic, morbidity was between 90 and 100% for both sheep and goats, but goats showed a mortality rate of 42%, compared with 18% in sheep (Amjadi and Ahourai 1975). In Israel, the morbidity rate was also higher in affected goats than sheep, with goat mortality as high as 44% in some herds (Van der Hoeden 1953).

In other domestic animal species, notably cattle and swine, there are known to be host-adapted serovars that are associated with subclinical infection and reproductive problems, as well as non-host-adapted or incidental sero- vars more likely to produce acute, clinical disease.

The goat is most likely exposed to infection from wild rodents or other infected livestock shedding the organism in urine (Schollum and Blackmore 1981). However, goats with acute infections can shed the organism in urine for at least one month after recovery and should be considered as potential sources of new infections during that time. Goats subclinically infected with host-adapted serovars may be chronic carriers.

Leptospires most commonly gain entrance to the host through skin or mucosal abrasions. They are readily killed by drying, but thrive under warm, moist conditions and will persist in contaminated standing water for long peri­ods. In the Iranian epizootic, the outbreak was attributed to a period of frequent rain, flooding, and warm weather that favored the environmental survival and spread of lepto- spires. In the Israeli report, the incidence of clinical cases fell off rapidly when the wet winter season ended and dry spring weather began. In Brazil as well, the occurrence of leptospirosis in goats is associated with increased rainfall (Alves et al. 1996).

Pathogenesis

Infection leads to a septicemic leptospiremia, followed by clearance of the blood as antibody response develops, and subsequent localization of the organism in the kidney with leptospiruria.

Clinical Signs

In acute leptospirosis goats may show a fever of 40-41.5 °C (104-106.7 °F), marked depression, and inappetence after an incubation period of four to eight days. Heart rate is increased and the animals are dyspneic. Icterus of mucous membranes is a prominent finding, and petechial hemor­rhages of the conjunctivae may be observed. Reddish brown urine indicative of hemoglobinuria is evident. Diarrhea has been reported in some cases. Lactating does will show a sharp drop in milk production and pregnant animals often abort. In untreated animals, death can occur within two to three days. Subclinical infections commonly occur in seemingly unaffected herd mates. Subclinical lep­tospirosis also occurs in goats and may be associated with abortions.

Clinical Pathology and Necropsy

In acute leptospirosis, a moderate to severe hemolytic anemia develops concurrently with the onset of clinical signs, and hemoglobinuria is present. In animals that do not die, there is soon evidence of a regenerative erythroid response. Leukopenia occurs during the acute phase of disease in cattle, but has not been reported in goats. Thrombocytopenia can occur in all affected species, with or without evidence of concurrent disseminated intravas­cular coagulation (DIC).

At necropsy, icterus is pronounced and extensive in acute leptospirosis (Amjadi and Ahourai 1975). Edema and ecchymosis of the subcutis and serous membranes occur. Lungs may be pale and edematous, widening of the inter­lobular septa occurring with yellow serous fluid.

Diagnosis

Definitive diagnosis depends on isolation of the organism and identification of the serovar. During the leptospiremic phase, the organism may be isolated from blood, but only with difficulty. The potential for isolation from the urine during the leptospiruric phase is somewhat better. It is advised to initiate cultures from fresh specimens right at the farm by inoculating a suitable transport medium. The need for culture has been obviated by the development of molec­ular techniques such as PCR, which can detect leptospiral DNA in tissues, blood, and urine (Hamond et al. 2014). In abortion cases, fetal kidney, lung, and pleural fluid should be examined microscopically for leptospires using silver stains, immunofluorescence techniques, or PCR.

Serologic tests are useful in leptospirosis for surveillance, prevalence studies, and establishing infection at the herd level. The microscopic agglutination test (MAT) is most commonly used. The MAT can also be used for confirming individual infections on the basis of a rise in antibody titer between acute and convalescent serum samples taken 7-10 days apart in clinically affected animals. The MAT measures both IgM and IgG antibody and is more useful in the diagnosis of acute disease than chronic disease. The range of positive titers observed in goats during outbreaks of abortion was 1 : 200 to 1 : 12800 using the MAT (Leon- Vizcaino et al. 1987). In Israel, titers of 1 : 100 were com­monly encountered in animals with no history of clinical leptospirosis. Therefore, titers of 1 : 300 or more were con­sidered as evidence of active infection. A titer of 1 : 30 000 was reported as early as day four of illness in a goat (Van der Hoeden 1953).

Where both diseases occur, babesiosis must be ruled out because of the similar presentation of hemolytic anemia, fever, and possible abortion. Identification of characteristic piroplasms in RBCs would confirm babesiosis. Anaplasmosis may also produce fever, anemia, and abortion, but icterus and hemoglobinuria are uncommon. Other differential diagnoses for hemolytic anemia with hemoglobinuria include copper toxicosis and plant intoxications, especially kale poisoning.

Treatment

Goats with acute leptospirosis have been reported to respond to a combination of streptomycin and penicillin (Amjadi and Ahourai 1975). In other species, streptomycin used at a dose of 12 mg/kg IM twice a day for three days controls the septicemia. A single IM injection of 25 mg/kg of streptomycin may clear leptospires from the kidney in the subsequent leptospiruric phase. A single IM injection of long-acting oxytetracycline at a dose of 20 mg/kg bw may be effective where the use of streptomycin in food ani­mals is prohibited. Note that, in goats, IM injection of oxy­tetracycline should be avoided, as it can be damaging to muscle and nerves at the injection site. The subcutaneous (SC) route is preferred.

Supportive therapy must be considered in acute leptospi­rosis, because anemia can be severe and the potential for renal failure is high due to primary interstitial nephritis and secondary hemoglobinuria with cast formation. Continuous IV fluid therapy is indicated to maintain renal output, and blood transfusions may be considered when the degree of anemia appears life-threatening.

Control

Early recognition and initiation of streptomycin or tetracy­cline therapy may reduce the number of clinical cases. Concurrent use of vaccination with the appropriate sero­type vaccine in the face of an outbreak has been shown to reduce the incidence of new cases and abortions in cattle. Active and recovered cases should be isolated because of the possibility of organisms continuing to be shed in the urine.

Always remember that leptospirosis is a potential zoono­sis. Observe appropriate hygienic procedures and counsel animal keepers to do the same. Two epidemiologic studies designed to identify risk factors for clinical human lepto­spirosis identified contact with goats as a significant risk factor. In Jamaica, the three main risk factors were contact with rodents, contact with goats, and being engaged in out­side labor (Keenan et al. 2010). In Nepal, owning goats, working in rice fields, and being male were the main risks (Shrestha et al. 2018).

Prevention is based on environmental hygiene measures such as rodent control, elimination of standing water, and avoidance of damp bedding; screening or prophylactic treatment of newly acquired animals for elimination of the carrier state; and vaccination. Little or no protective cross­immunity occurs among the various leptospiral serovars, so vaccination should be based on serologic evaluation of prevailing serovars. Multivalent vaccines suitable for use in goats are available and in some countries are specifically approved for use in goats. All animals older than 3 months of age should be vaccinated. Kids of vaccinated dams nurs­ing colostrum should be protected by passive antibody up to 3 months of age. Initial vaccinations should be followed by a booster four to six weeks later and then a single dose given annually. When considering vaccination, bear in mind that leptospirosis in goats is uncommon, and the cost-to-benefit ratio of routine vaccination for leptospirosis in goats is not known. In an American study undertaken to evaluate the health status of goats in relation to manage­ment practices in 43 herds, no cases of leptospirosis were reported in any of the herds, regardless of whether they were vaccinated (Hagstad et al. 1984). The prevalence of leptospirosis in the practice area should be assessed in con­sideration of vaccination programs. Farmers, herders, vet­erinarians, milkers, and slaughterhouse workers have an increased occupational risk of exposure to this zoonotic disease and should exercise appropriate hygienic precau­tions to prevent infection.

Anthrax

Anthrax is a well-known infectious disease of livestock with zoonotic potential. The disease in goats is very similar to that in other ruminant species. This septicemic condi­tion is characterized by a failure of the blood to clot. This is commonly noted at death by a bloody discharge from the nose and mouth.

Etiology and Epidemiology

Bacillus anthracis is the cause of anthrax in herbivores and humans. The organism is characterized by the ability to produce spores, on exposure to air, that are capable of per­sisting for longer than 50 years. Anthrax is endemic in many tropical and subtropical regions of the world. The major route of transmission in animals is ingestion of spores residing in soil during periods of grazing. The dis­ease has a seasonal occurrence and is predisposed by envi­ronmental temperatures exceeding 15 °C (59 °F), periods of drought, or heavy rains. Goats are susceptible to anthrax, but reports of the condition in goats are uncommon, per­haps because they are not ground-grazing animals by nature. Outbreaks involving goats have been reported from Nigeria (Okoh 1981), Texas (Whitford 1982), China (ProMED-mail 2006), Ethiopia (Shiferaw 2004), Italy (Palazzo et al. 2012), Tanzania (Mwakapeje et al. 2017), and India (Dabbir 2019), and are possible wherever anthrax is endemic in other species. Grazing is not an absolute pre­requisite for exposure to anthrax. Zero-grazed goats in

Texas that were fed hay and a pelleted feed were confirmed with anthrax (ProMED-mail 2008). It is presumed that one or more of the provided feeds was contaminated with anthrax spores. Additional information on the epidemiol­ogy of anthrax is available elsewhere (Constable et al. 2017).

Clinical Findings and Diagnosis

The disease is most commonly characterized by a peracute, fatal course, with most affected animals found dead, the result of bacteremia and toxemia. In acute cases, goats may be noted to be salivating and extremely depressed, with the head hanging down. Over a period of one to two days they become recumbent and moribund and die. Observation of bleeding from the nostrils and mouth of dead animals is characteristic of anthrax. Carcasses of suspect animals should not be opened at the site of death, because this will release spores that will contaminate the environment. If movement of the carcass is not possible, then carefully aspirated blood samples and superficial lymph node aspi­rates can be taken and submitted for bacterial culture. If necropsy is performed, the blood is unclotted and the spleen is dramatically enlarged. Hemorrhages on serosal surfaces suggestive of septicemia are observed. The organ­ism can be cultured from tissue. The differential diagnosis must include all potential causes of sudden death, as dis­cussed in Chapter 16.

Treatment and Control

Peracute and acute cases of anthrax carry a grave progno­sis. When goat herds have been exposed to anthrax spores and clinical cases are seen, further losses may be prevented by prophylactic treatments of the remaining exposed ani­mals, noting however that some jurisdictions do not allow the treatment of animals with anthrax. A wide range of antibiotics including tetracyclines, aminoglycosides, qui­nolones, macrolids, and beta lactams are all likely to be effective in this regard. Penicillin has long been the drug of choice because of its effectiveness, ready availability, and low cost. Procaine penicillin can be given at a dose of 44 000 IU∕kg bw IM once a day for two days. Other beta lactams are also effective, such as long-acting amoxicillin at a dose of 15 mg/kg bw or a combination of ampicillin and cloxacillin at a dose of 10 mg/kg bw. Though B. anthra- cis is known to be capable of producing beta lactamase, this has not been associated with failures of beta lactam ther­apy in the field for treatment of anthrax in animals (WHO 2008). Historically, anthrax hyperimmune serum has been administered as a treatment in the face of an out­break and, where available, can be effective.

Live, attenuated spore vaccines are available for preven­tion or control of anthrax. These vaccines are usually derived from the 34F₂ “Sterne” strain. When vaccinating in the face of an outbreak, vaccine should be given to animals not showing any signs. Animals showing signs should be treated with antibiotics. If antibiotics are given, an interim of 7-10 days should be observed before any subsequent vaccination is administered so as not to diminish vaccine efficacy.

For prevention in endemic areas, anthrax vaccines are usually given annually. Goats are prone to adverse reactions (progressive edema) after receiving the Sterne vaccine and it should be used with caution in goats. To minimize the risk, it has been suggested that an initial schedule of two inoculations one month apart be observed, with the first dose being one-quarter of the standard recommended dose and the second dose being the standard recommended dose. A single annual booster may be administered thereafter (WHO 2008). In goats the vaccine should be given SC in the flank or tail fold rather than the neck.

Anthrax is an important zoonotic disease. Transmission is usually by direct handling of hair, wool, skins, or car­casses of infected or contaminated animals. The disease can also be spread by inhalation of spores. A textile mill worker in North Carolina was diagnosed with anthrax that was traced to handling cashmere goat hair imported from endemic regions of western Asia (Briggs et al. 1988). Cases of cutaneous and inhalation anthrax in humans have been reported in the United States in association with the han­dling of goat skins imported from Africa for drum-making (Kaplan 2007). There are numerous reports from develop­ing countries of human cases of anthrax occurring among villagers who eat meat from livestock that have died of anthrax, including goat meat (Boutin et al. 1985; ProMED­mail 2006). Suitable personal protective equipment should be worn when handling carcasses or animal products sus­pected of being contaminated with anthrax. Animals dying of unknown causes or of suspected anthrax should not be eaten. Carcasses should be burned or buried deeply to avoid dissemination and persistence of spores in the environment.