Bacterial Diseases of Goat and Its Preventive Measures

*Kumaragurubaran Karthik and Manimuthu Prabhu*

### **Abstract**

Bacterial diseases of goats can cause huge economical loss to the farmers. Due to intensification of goat farming and poor hygienic practices there is increase in the number of bacterial diseases that affect the goats. Diseases like tuberculosis, Johne's disease and Brucellosis are chronic diseases that may be identified in the initial stages of infection during which they spread to other animals. Similarly, brucellosis, tuberculosis and also anthrax are zoonotic diseases hence due consideration has to be provided while handling animals suspected for these diseases. Use of vaccine before onset of the disease in endemic areas can prevent the disease outbreak and spread to other naïve population. Good hygienic practices and biosecurity measures at farm are essential to prevent disease spread. The present chapter deals with various bacterial diseases affecting goats and its preventive measures. This chapter can be a guide to field veterinarians, students and farmers as it highlights the important bacterial diseases of goats.

**Keywords:** Goat, Bacterial disease, Brucella, Anthrax, Preventive measures

### **1. Introduction**

Due to intensification of small ruminant farming, there is increase in the number of disease outbreaks in the recent years. Among the various infectious diseases, diseases caused by bacterial pathogens contribute to severe economic loss to the goat farmers. Various factors like increase in herd size, reduced ventilation in farm and poor husbandry practices can predispose to diseases. Bacterial diseases like anthrax, enterotoxaemia, tetanus, gas gangrene, caseous lymphadenitis, listeriosis, tuberculosis, Johne's disease, dermatophilosis, pasteurellosis/mannheimiosis, brucellosis, foot rot, contagious caprine pleuropneumonia, colibacillosis, salmonellosis, etc., affect goats and can cause various ailments and some diseases can cause heavy mortality leading to huge economic loss to the farmer [1]. Different bacterial pathogens affect different organs of goat thereby eliciting various clinical signs based on which a tentative diagnosis can be made (**Figure 1**).

Antibacterial agents can be used to treat various bacterial diseases but these drugs should be used judiciously due to the risk of development of antimicrobial resistance. Vaccination is the best way to prevent infectious diseases and based on the pattern of the disease annual vaccination should be practiced to prevent disease outbreaks. Diseases like anthrax, brucellosis and tuberculosis pose threat to human since these diseases can be transmitted to human through direct or indirect route of transmission [2]. Due care should be taken while handling infected goats or dead goats in farm as the zoonotic diseases can cause severe aliments in human.

#### **Figure 1.**

*Different bacterial diseases of goat and the organ/ tissues affected. Brucellosis affects reproductive tract, dermatophilosis affect the skin, johne's disease causes corrugation of intestine, pasteurellosis/ mannheimiosis, tuberculosis, contagious caprine pleuropneumonia affects the respiratory system, caseous lymphadenitis affects the lymph nodes and tetanus affects the nervous system. This figure is propriety of the authors.*

### **2. Methods**

This chapter is a comprehensive summary of important bacterial diseases of goats and this can be a guide to veterinary students, field veterinarians and goat farmers regarding the impact of these bacterial diseases. This chapter also highlights the preventive measures and zoonotic potential associated with the bacterial diseases of goats. Important bacterial diseases that are zoonotic and economically important like anthrax, brucellosis, tetanus, enterotoxaemia, Johne's disease, Pasteurellosis/ Mannheimiosis, caseous lymphadenitis, contagious caprine pleuropneumonia, dermatophilosis and foot rot are discussed. Each disease is delt with various subsections like definition of the diseases, etiology, epizootiology, transmission clinical signs, diagnosis, treatment, preventive measures and public health significance, if any.

#### **3. Anthrax**

Anthrax is a peracute, acute or subacute, often fatal disease of animals including goats. In goats the disease is mainly characterized by septicaemia, splenomegaly and gelatinous infiltration of subcutaneous or subserosal tissues. The disease is commonly known as woolsorter's disease, splenic fever, charbon, and milzbrand.

#### **3.1 Etiology**

The disease is caused by *Bacillus anthracis*, a gram positive, capsulated, non-motile, aerobic, spore-forming, rod shaped bacterium [3].

#### **3.2 Epizootiology**

The disease is worldwide in distribution and is endemic in some countries, while occurs in defined regions of other countries. It was reported to be associated *Bacterial Diseases of Goat and Its Preventive Measures DOI: http://dx.doi.org/10.5772/intechopen.97434*

with heavy mortalities in goats and sheep of sub-saharan region in 1960–70s and in other countries. In recent days, through strict vaccination procedures the incidence reduced in most countries, however, sporadic cases are still being reported. *B. anthracis* is widely distributed in the environment, as they produce highly resistant endospores. They can tolerate extremely adverse conditions such as desiccation, high temperatures and chemical disinfectants. When the vegetative bacteria are exposed to atmospheric oxygen under favorable temperature (20–40°C) and relative humidity (>60%), the spores are formed. Further, the calcium plays a role in spore formation and in combination with dipicolinic acid, enhances the spore survival. Hence, its survival is more in alkaline soil that is rich in calcium and nitrogen and with high moisture content, the endospores can survive for more than 50 years. Further, recurrent cycles of flooding and evaporation may concentrate spores in particular low-lying regions [3].

### **3.3 Transmission**

Goats are infected by ingestion of food, water or soil contaminated with spores. The infection can also occur through inhalation or abraded skin and oral mucosa. Mechanical transmission by biting insects is also reported. Wild animals acting as carriers makes the control programme challenging as it is least possible to vaccinate all wild animals.

#### **3.4 Clinical signs**

The incubation period ranges from hours to days. The disease is usually fatal, especially in sheep and goats, after 1–3 days. The peracute case is characterized by sudden death without any premonitory signs. However, there may be fever, dysponea, congestion of mucous membranes, muscular tremors and terminal convulsions in few animals. In acute cases, fever, anorexia, labored breathing, increased heart rate, ruminal stasis and reduce milk production may be observed. There may be bloody discharges from orifices like mouth, nostrils, anus and/or vulva. Diarrhea or dysentery and oedema and swelling of the tongue, throat, flank and perineum (anus, vulva) may be seen. Pregnant animal abort and blood-tinged milk is produced. Animals then collapse with terminal convulsions and die [4].

Necropsy of suspected carcass is not recommended, as the vegetative bacteria may get transformed into spore and hence contaminate the environment. The pathological features such as absence of rigor mortis and rapid putrefaction and bloating of the carcass are common clinical features. Oozing of unclotted dark, tarry colored blood from orifices, soft and enlarged spleen, blood-stained fluid in body cavities and widespread ecchymotic hemorrhages are frequently observed post mortem findings.

#### **3.5 Diagnosis**

Though clinical signs are highly suggestive, the diagnosis based on clinical signs alone is difficult. Thin smears of blood from ear tip can be stained with polychrome methylene blue stain to reveal short chains of truncated blue color rods, surrounded by pink capsules (McFadyean reaction). The organism can be cultured on Sheep or Ox blood agar which shows flat, dry grayish colonies with 'ground glass' appearance after 24–48 hours of incubation (**Figure 2**). The selective media for the organism is PLET (Polymyxin-lysozyme-EDTA thallous acetate) medium. The Ascoli's thermoprecipitation test is also commonly used test to detect antigens of *B. anthracis*. Agar gel immunodiffusion, complement fixation test, ELISA and immunofluorescence

**Figure 2.** *Ground glass appearance Bacillus anthracis colonies on sheep blood agar. This figure is propriety of the authors.*

tests though available are insensitive and not routinely used [4]. The PCR test can be used for direct detection of the organism from decomposed samples and can also be employed for targeting the pXO1 and pXO2 plasmids to confirm the virulence of isolates from the culture.

#### **3.6 Treatment**

Ailing animals in early stages of infection can be treated with penicillin or oxytetracycline or other long-acting antibiotics. An anthrax antiserum may result in recovery if used in early stages. Vaccination should follow 7–10 days after the conclusion of antibiotic therapy [4].

#### **3.7 Preventive measures**

In endemic areas, annual vaccination is advisable. The goat should be vaccinated with 'Sterne strain' live spore vaccine one month before the anticipated outbreaks. In non-endemic areas, movement of animals and their products should be restricted; feed and bedding materials etc., should not be transferred from affected herds. Disinfection of the premises with 5% formalin, 5% sodium hydroxide or 3% peracetic acid and placing foot-baths containing these sporicidal disinfectants at the entrances of the affected farms will help to control the spread of infection. Contaminated building should be fumigated with formaldehyde before removing the bedding materials [5]. Proper disposal of carcasses and the infected materials should be done either by deep burial or incineration.

#### **3.8 Public health significance**

*B. anthracis* is considered a bioterrorism agent. Three forms of disease occur in human beings. When endospores enter through abraded skin, the cutaneous form of anthrax (malignant pustule) develops. While, the pulmonary form (woolsorters' disease) follows inhalation route and intestinal form results from ingestion of infective material. The disease usually fatal if not treated early [6].

### **4. Brucellosis**

Caprine brucellosis is an infectious zoonotic disease having substantial economic impact on both livestock and human. Caprine brucellosis is reported since ancient days; Hippocrates II first described the human brucellosis in 400 B.C. which was most likely to be associated with consumption of raw milk or derivatives of infected sheep or goats.

### **4.1 Etiology**

The causative agent is *Brucella* species mainly *B. melitensis* that are small, nonmotile, non-spore forming, gram-negative coccobacilli. Goats are also susceptible to infection by *B. abortus,* particularly when housed in close proximity with infected cattle; however, they do not sustain the infection in the herd [7].

### **4.2 Epizootiology**

The disease is prevalent worldwide and it remains a major burden in parts of Mediterranean region, the Middle East, Central and Southeast Asia (including India and China), sub-Saharan Africa, and parts of Latin America [8]. Goat herds from USA, Canada, Colombia, Chile, and Uruguay are reported to be free from *B. melitensis* infection.

### **4.3 Transmission**

Infection occurs primarily through ingestion of the organisms. Goats acquire infection by licking the aborted fetuses, placentas, newborn kids, vaginal discharges, or by consumption of feed contaminated with these infectious materials [9]. Milkers can also spread the infection through unsanitary milking practices.

### **4.4 Clinical signs**

The disease is more severe in goats and is protracted than in sheep. Clinical manifestations include high abortion rates particularly during the fourth month of pregnancy and retained placentas, orchitis in bucks, arthritis and hygromas. In goats, mastitis and lameness may also be seen. The abortion rate can be high when this bacterium first enters a naive flock or herd [10]. The abortion rates are usually much lower once *B. melitensis* has become established in a herd and only a few animals abort repeatedly but affected animals shed bacteria during parturition. Healthy asymptomatic carriers become a potential source of infection. Other clinical signs include death of weak offspring, low weaning weight, decreased milk production, and epididymitis, and reduced fertility which is more common in sheep. In case of abortions, fetus might reveal excess of bloodstained fluids in the body cavities, with enlarged spleen and liver. Moreover, infected foetal membranes can show thickened and dull-gray color necrotic cotyledons [11].

### **4.5 Diagnosis**

Diagnosis is made based on clinical signs, direct examination of MZN-stained smears of fluids or tissues, isolation and identification of *B. melitensis* from milk or an aborted fetus or by serum agglutination tests. The Rose-Bengal agglutination test and the complement fixation test are the most widely used methods for detecting *B. melitensis* infection and are approved for international trade. Indirect enzymelinked immunosorbent assays (ELISA) have been developed and are also approved tests for the purposes of international trade [12]. Isolation and identification of *B. melitensis* from aborted foetal stomach contents, placenta and uterine fluids can be

**Figure 3.** *Brucella melitensis colonies on sheep blood agar. This figure is propriety of the authors.*

attempted and isolation is the gold standard technique for confirmation of brucellosis (**Figure 3**). Isolation should be carried out in biosafety cabinet class III as the organism is zoonotic.

### **4.6 Preventive measures**

Test and slaughter policy of the infected herd is generally implemented in countries where the disease is considered exotic. This can also reduce the prevalence of disease in endemic areas. In most countries where *B. melitensis* is endemic, vaccination with the Rev. 1 strain is commonly employed [13]. It is a live attenuated strain of *B. melitensis*; administered by the subcutaneous or conjunctival routes and is used for vaccination of kids and lambs up to 6 months of age.

### **4.7 Public health significance**

*B. melitensis* is highly pathogenic than other species of Brucella for human beings. The infection in human is characterized by fever, chills, headache, malaise, back pain, myalgia and lymphadenopathy, which may be accompanied by splenomegaly and/ or hepatomegaly. The patients may experience drenching sweats at night and nonspecific gastrointestinal signs such as vomition, diarrhea and/or constipation [14]. Localized manifestations such as arthritis, spondylitis, sacroiliitis, osteomyelitis, bursitis and tenosynovitis may be observed. Epididymo-orchitis, prostatitis and seminal vesiculitis can be seen in males, whereas abortion or premature births are seen in pregnant women. Deaths are usually uncommon except in infants caused by endocarditis or infections of the brain.

### **5. Tetanus**

Tetanus (Lockjaw) is an acute, highly fatal intoxication of all domestic animals and humans caused by neurotoxin produced by the bacteria *Clostridium tetani* [15]. Though all species of livestock are susceptible, sheep and goats are more susceptible than cattle and horses being the most susceptible. It is characterized by hyperasethesia, tetany and convulsions.

### **5.1 Etiology**

The etiological agent, *Clostridium tetani* is a strictly anaerobic, motile, slender, straight, spore forming ('drumstick appearance'), Gram-positive rod. Based on flagellar antigens, so far 10 serotypes of *C. tetani* have been described and all produce antigenically a similar neurotoxin called tetanospasmin. Though endospores are resistant to chemicals and boiling, they are destroyed by autoclaving.

### **5.2 Epizootiology**

Tetanus is worldwide in distribution and occurs sporadically. The organism is normal inhabitant of intestinal tract of animals and persists as resistant spores in soil, manure [16].

### **5.3 Transmission**

The toxemia in tetanus is caused by a specific neurotoxin produced by *C. tetani* in necrotic tissue. Spores are introduced into the tissue through wounds, specifically deep puncture wounds that provide the favorable anaerobic environment. Most outbreaks occur following mass contamination of animals during castration, vaccination, ear tagging, docking and other surgical procedures [17]. Grazing on rough and spiky pastures may injure the oral mucosa and hence may facilitate the invasion of the bacteria. The spores remain dormant in tissues and proliferate to liberate toxins under favorable conditions.

### **5.4 Clinical signs**

The incubation period is usually of 4 days to 3 weeks. The initial signs include muscle stiffness, tremors and prolapse of the third eyelid. This is followed by rigidity and extension of the limbs leading to a stiff gait and abnormal flexion of the joints. Tetany of masseter muscles causes drooling of saliva (lock jaw) and regurgitation through nostrils [17]. The animals may exhibit bloat, an inability to chew, and hyperthermia. Retracted lips, hypersensitivity to external stimuli, and a 'saw-horse' stance are frequent signs. The spasms of alimentary and urinary tract muscle may cause constipation and retention of urine [17]. The abnormal muscular contracture may result in opisthotonus, curvature of the spine and bending of the tail. The disease is highly fatal and death occurs within 3–10 days with mortality nearing 100%, primarily as a result of respiratory failure. Necropsy features usually are nonspecific except for the inflammatory reaction associated with the wound.

### **5.5 Diagnosis**

Diagnosis can be made based on clinical features such as muscular spasms, prolapse of third eyelid and based on history of trauma or surgery. The Gram-positive rods with terminal spores can be demonstrated in the smears prepared from necrotic tissue or wound [18]. Anaerobic culture of the bacteria from necrotic tissue may be attempted but is often unsuccessful. PCR and real-time PCR techniques can be employed for the detection of neurotoxin genes of the organism. Mouse inoculation test can be performed to demonstrate circulating neurotoxin from the serum of affected animals.

### **5.6 Treatment**

Treatment mainly aimed at wound management, antibiotic therapy, antitoxin administration and vaccination. Wound management consists of surgical debridement of infected wounds and removal of debris, flushing with hydrogen peroxide to produce aerobic condition that helps to inhibit replication of the bacteria at the site of infection. The antibiotics (large doses of Penicillin) can be given both parenterally and flushed into the cleaned wound to prevent further replication of the bacteria and production of toxin [19]. Affected animals must be kept in a quiet and dark environment. Fluid replacement therapy, sedatives and muscle relaxants can minimize clinical discomfort and maintain vital functions. To neutralize unbound toxin, the tetanus antitoxin must be administered on time, either intravenously or into the subarachnoid space for three consecutive days. Vaccination with tetanus toxoid may be given subcutaneously to promote an active immune response even in those animals that are treated with antitoxin.

### **5.7 Preventive measures**

Tetanus can be controlled by following good sanitation measures, aseptic surgical and management procedures and vaccination. Goats in a herd must be vaccinated routinely with tetanus toxoid which is very effective for stimulating long-term immunity. They can be vaccinated 2–3 times during the first year of life followed by booster vaccination before parturition to ensure colostral antibodies [20]. Further, a booster dose may be advisable if a vaccinated animal sustains a deep wound.

### **6. Enterotoxemia**

### **6.1 Etiology**

Enterotoxaemia in goats is caused by *Clostridium perfringens,* a gram-positive, non-motile, spore-forming bacilli that grows well in anaerobic or micro-aerophilic conditions. This disease condition tends to be associated mainly with sheep and is of less importance in goats and cattle. *C. perfringens* Type D primarily produce enterotoxamia and Type C sometimes causes sudden death in goats. Grain-fed kids (3–12 weeks old) on a high-concentrate diet are most susceptible, but adult goats may also be affected. Goats are commonly affected with a hemorrhagic form of enterotoxemia.

### **6.2 Epizootiology**

*C. perfringens* is worldwide in distribution and is found in soil, feces, and in the intestinal tracts of animals and humans. *C. perfringens* types B, C and D may survive in soil as spores for several months. *C. perfringens* type A constitutes a part of the normal intestinal flora and is widely dispersed in soil. Overcrowding and prolonged confinement may increase the spread and severity of the condition.

#### **6.3 Transmission**

The *C. perfringens* type D is found as obligate parasite in the intestinal tract of animals [21]. The animals on a high grain diet or on succulent pasture are predisposed to this condition (hence described as 'over-eating disease'). Thus, the disease is more common in well-fed animals in intensive feedlots.

### **6.4 Clinical signs**

The peracute condition is characterized by sudden death of younger and healthy kids. This is occasionally preceded by other signs such as loss of appetite, lack of rumen activity and rumination, bloat, depression and a drunken appearance; the animals may show neurological signs such as incoordination, inability to stand, and convulsions. There may be watery diarrhea and glucosuria. In goat's acute disease is mainly characterized by dysentery, abdominal discomfort and convulsions.

In acute cases of goats, the necropsy findings include pulmonary edema, necrosis of intestinal walls and scattered hyperaemic areas of intestine. Intestinal contents may be green, blood-stained or mucoid, and fibrinous casts may be present in the lumen of the large intestine [22]. Mesentric lymph nodes may be edematous. Fluid accumulation in the pericardial sac, extremely necrotic, soft kidneys ('pulpy kidneys'), focal encephalomalacia, and petechiae of serosa of the brain, diaphragm, gastrointestinal tract and heart are common findings.

### **6.5 Diagnosis**

Diagnosis of enterotoxaemia depends on epidemiological features, type of diet, clinical and pathological features. Gram positive rods can be demonstrated in the smears of intestinal contents or in the lesions of intestine. The culture of bacteria from fecal samples in cooked meat media may be suggestive of the disease (**Figure 4**). Organism on blood agar plates show double zone of hemolysis which is suggestive of *C. perfringens*. Demonstration of the epsilon toxin in the intestinal content is highly reliable method. Protection of mice injected with infiltrates of toxin from intestinal contents against specific antisera is diagnostic. Genotyping by PCR can be used to type isolates of *C. perfringens* as an alternative to in vivo toxin neutralization tests.

#### **Figure 4.** *Double zone hemolytic colonies of Clostridium perfringens on sheep blood agar. This figure is propriety of the authors.*

Though ELISA tests can be performed, misdiagnosis may occxur as this test detects low levels of toxin in the intestinal contents of normal animals [23].

#### **6.6 Treatment**

Treatment generally is ineffective as most cases are acute in nature. A hyperimmune serum, if available, can be used and a combination of hyperimmune serum along with sulphadimidine has been found useful in goats. Chelating agents can be used to neutralize toxins [21].

#### **6.7 Preventive measures**

Vaccination before the anticipated outbreaks is the primary method of control. Alum precipitated formalin killed whole culture toxoid vaccines are commercially available. In ruminants, maternal antibodies last about 5–6 weeks postpartum and hence, the young animals must be vaccinated at this time. Kids are usually vaccinated twice at 4 weeks interval and then re-vaccinated at once in 6 months. However, several anaphylactic reactions have been reported in Sannen kids re-vaccinated with toxoids [24]. Sudden dietary changes and other predisposing factors to enterotoxaemias must be managed. Feeding regimens and feeding of concentrates even to adult goats should be monitored carefully.

### **7. Johne's disease (JD)**

A chronic, contagious, granulomatous disease affecting small intestine of adult ruminants and the affected animals show weight loss and intermittent diarrhea [25].

#### **7.1 Etiology**

JD is caused by *Mycobacterium avium* subspecies *paratuberculosis*, a fastidious, acid-fast, gram-positive rod [25].

#### **7.2 Transmission**

The organism is present in the environment and animals at young are affected either through ingestion of contaminated milk or direct contact. Infected goats may excrete the bacteria in the feces thereby contaminating the environment [26].

#### **7.3 Clinical signs**

The incubation period is usually months to years. Chronic wasting is a characteristic sign in goat and at times pasty feces or diarrhea (in advanced cases) can be witnessed. In advanced cases the animals may lose weight rapidly and will have a hide and bone condition. During PM examination intestine of the affected animals have a corrugated appearance [27].

#### **7.4 Diagnosis**

Affected animals can be identified in the herd by intradermal skin testing using Johnin purified protein derivative (PPD). Alternatively, Interferon gamma assay (IGRA) can also be used to assess the cellular immunity. Lymph nodes (Ileal and ileocecal) aspirates, intestinal scrapping can show acid fast bacilli in staining

**Figure 5.** *Acid fast bacilli in intestinal scrapping. This figure is propriety of the authors.*

(**Figure 5**). Organism my shed intermittently in feces and hence, bacilli can be found by acid fast staining [27]. Organism can be detected intestinal tissues, lymph node and feces by culture and PCR. Detection of antibody in the later or final stages of the disease can also be attempted for diagnosis.

### **7.5 Treatment**

Treating animals with antimycobacterial agents are not fruitful.

### **7.6 Preventive measures**

Due to its chronic nature, it is difficult to identify the disease early hence, it is advised to test a newly purchased animal before letting into the farm. Test and cull policy is better to break the chain of infection. Suspected animals should be separated from the herd and affected animals milk should not be fed to neonates [25]. The organism may survive longer in the pasture hence, once an animal is found positive it is best to change the pasture land.

### **7.7 Public health significance**

A similar condition in human named as Crohn's disease has been suspected to be caused by *Mycobacterium avium* subspecies *paratuberculosis* still there is no clear evidence for zoonotic transmission of the pathogen [28].

### **8. Pasteurellosis and Mannheimiosis**

Pasteurellosis and Mannheimiosis is an acute fatal disease characterized by pneumonia and septicemia.

### **8.1 Etiology**

*Pasteurella multocida* and *Mannheimia haemolytica* are aerobic, bipolar, nonmotile, non-spore forming gram-negative rods [29].

### **8.2 Epizootiology and transmission**

*P. multocida* and *M. haemolytica* are ubiquitous and even present in respiratory tract of healthy animals. Young animals are prone to infection than adults. Stress including weaning, transportation (hence termed as shipping fever), change in diet/weather and overcrowding are the predisposing factors for the condition. Viral diseases can also predispose Pasteurellosis and Mannheimiosis and the organism can be transmitted directly or indirectly through inhalation or ingestion [30].

### **8.3 Clinical signs**

Acute rhinitis or pharyngitis is the common sign noticed in animals. Animals may have high fever, anorexia, and rapid breathing along with profuse mucopurulent nasal/ ocular discharges. Kids are more susceptible than adult goats and death may occur without any clinical signs [30]. PM changes include marbling of lungs, pleural adhesion, sero-fibrinous fluid in the thorax, frothy exudate in trachea and also in bronchi.

### **8.4 Diagnosis**

Bipolar organisms of *P. multocida* can be noticed in the impression smears from dead animals (**Figure 6**). Isolation of the organism on selective media and biochemical confirmation is the standard diagnostic procedure. *M. haemolytica* produces hemolytic colonies on blood agar and it can grow on MacConkey agar which are the differentiating features from *P. multocida*. Molecular diagnosis can be carried out by PCR [31].

### **8.5 Treatment**

Use of antibiotics based on antimicrobial susceptibility testing can be used to control the bacterial propagation and anti-inflammatory agents can be used to control fever [30].

### **8.6 Preventive measures**

*M. haemolytica* and *P. multocida* bacterins can be used as vaccines to prevent the occurrence of the disease [32]. Other measures like reducing overcrowding thereby improving the ventilation in enclosures and also reducing the stress during transportation can prevent the occurrence of the disease.

## **9. Caseous lymphadenitis**

Caseous lymphadenitis (CLA) is contagious, subclinical and chronic suppurative condition of sheep and goats, occasionally in cattle and is characterized by the formation of abscesses in lymph nodes and visceral organs [33].

### **9.1 Etiology**

CLA is caused by *Corynebacterium pseudotuberculosis*, small, non-motile, nonspore forming, pleomorphic, Gram-positive bacteria which may occur in curved, coccoid, club and rod forms (coryneform morphology) [33]. Two biotypes of *C. pseudotuberculosis* are recognized; ovine/caprine biotypes that lack nitrate-reducing capacity mainly affect sheep and goats, causing superficial and visceral abscesses. The second equine/bovine biotype usually reduce nitrate and mainly affects horses and cattle, causing ulcerative lymphangitis.

### **9.2 Epizootiology**

CLA is worldwide in distribution and the probable dissemination of the disease throughout the world occurred through importation of infected animal [34]. This disease is found in parts of North and South America, Australia, New Zealand, the Middle East, Asia and Africa and is being reported more often in Britain and other European countries.

### **9.3 Transmission**

The bacteria can survive in the environment for about 6 months or more. Transmission can occur either through direct or indirect contact or through wounds contaminated with pus from the abscesses of infected animals. The organism enters through contamination of skin wounds arising from castration, ear tagging or tattooing, docking or shearing operations. Arthropod bites or contaminated dips can also be the source of infection [34]. Goats having traumatized buccal mucosa have more chances of taking the bacterium from contaminated feed. The organism has also been isolated from the milk of affected goats.

### **9.4 Clinical signs**

The incubation period varies from weeks to months; usually is about 3 months. CLA may be manifested in two forms: in its superficial form it is characterized by infection of peripheral lymph nodes, such as the submandibular, parotid, prescapular and supramammary lymph nodes (**Figure 7**). These peripheral lymph nodes enlarge, may erode and eventually leads to formation of abscess in chronic cases. Visceral form is characterized by abscessation of internal organs, such as lungs, liver, kidneys, uterus, spleen and internal lymph nodes (mainly mediastinal and bronchial lymph nodes) that may not be detectable antemortem [35]. These two forms can co-exist; however, the visceral form is more common among sheep, while superficial form is more frequent among goats with external abscesses in the lymph nodes particularly of the head and neck regions.

Eventually, the affected animal become exercise-intolerant, anorectic, ill-thrift and debilitated (often known as thin-ewe syndrome in sheep). Fever, increased respiratory rates, and pneumonia may also be noticed. Morbidity up to 15% is common, and morbid animals will often eventually succumb to the disease. The infection can also lead to abortion in doe and orchitis and/or epididymitis in bucks.

**Figure 7.** *Lymph node enlargement in goats noted in caseous lymphadenitis. This figure is propriety of the authors.*

Though less common, orchitis can be acute in which the buck develops fever, reduced appetite, lack of walking ability and loss of libido. The infected testes appear swollen, hot and painful to touch.

### **9.5 Diagnosis**

Diagnosis is based on clinical signs and lesions and abscessation of both superficial and visceral lymph nodes is typical. Radiographs may be useful in identifying affected central nodes which also must be confirmed by culture of tracheal washings. Gram and Giemsa staining can be used for identification of the bacteria. Isolation of organism from purulent material from abscessed lymph nodes in case of live animals and /or from abscesses of internal organs from dead animals. ELISA tests which detect antibodies directed against either cell wall antigens or the exotoxin (Phospholipase D - PLD) are available [34]. Further, the detection of INF-γ by ELISA, an indicator of cell-mediated immunity, has also been potentially used for demonstration of CLA in eradication programs. Molecular techniques such as PCRs targeting 16S rDNA, *rpo* and *pld* genes have also been used in the recent years for the diagnosis of caseous lymphadenitis.

### **9.6 Treatment**

Though *C. pseudotuberculosis*, in vitro is susceptible to antibiotics, the antibiotic therapy is usually not much effective in animals. The chronic nature of infection, the intracellular location of the bacteria and the formation of biofilm in natural infections reduce the antibiotic efficacy, making them useless. Draining of abscesses, followed by cleansing and chemical cauterization with 10% iodine may be helpful or the localized abscesses may be removed entirely from valuable animals [34].

### **9.7 Preventive measures**

As CLA is contagious in nature, the animals with draining and punctured lesions should be kept isolated until healed. Reducing the environmental contamination, proper sanitation and biosecurity of facilities and instruments and safety measures to prevent injuries are all important in control. The causative agent is sensitive to

*Bacterial Diseases of Goat and Its Preventive Measures DOI: http://dx.doi.org/10.5772/intechopen.97434*

common disinfectants such as hypochlorite, formalin and cresol; however, the surfaces should be cleaned before disinfection, as organic matter usually interferes with the action of these agents. The control measures vary with the prevalence of infection. In countries with a high incidence, rigorous sanitary procedures must be implemented, along with vaccination. Disease eradication can be achieved in endemically-infected herds by test and disposal policy [36].

Most of the commercially available vaccines contain inactivated PLD of either *C. pseudotuberculosis* or of other pathogens, such as *Clostridium* species. Glanvac vaccine (Vetrepharm, Inc. London) is licensed for use in sheep and goats in Canada, Australia and New Zealand. However, the use of PLD toxoid in goats may result in some adverse consequences such as reduction in milk, fever, ventral edema, ataxia and convulsions; therefore, its use is restricted [34]. On the other hand, live vaccines targeting the attenuation of PLD gene, confers the best and longest-lasting immune response, due to its similarity to natural infection.

### **9.8 Public health significance**

Human beings are rarely affected, some cases of human infections have been documented as occupational infection in veterinary doctors and assistant as well as farm experts.

### **10. Contagious caprine pleuropneumonia**

Contagious caprine pleuropneumonia (CCPP) is a highly contagious and rapidly spreading mycoplasmal disease of goat, occasionally sheep and wild ruminants. CCPP is characterized by severe sero-fibrinous pleuropneumonia, very high morbidity (100%), and mortality (80–100%) and results in heavy economic losses.

#### **10.1 Etiology**

CCPP is caused by *Mycoplasma capricolum* subspecies *capripneumoniae* (Mccp), which was earlier known as *Mycoplasma* biotype F38. It belongs to the class *Mollicutes* that lack cell wall. *M. ovipneumoniae*, *M. mycoides* subspecies *capri*, and *M. mycoides* subspecies *mycoides* (Large Colony Type) are also considered as etiological agents of caprine pneumonia in the United States [1].

#### **10.2 Epizootiology**

CCPP is becoming a novel emerging and rapidly spreading disease in most parts of the world and at present, goat populations in more than 40 countries are affected with CCPP and sporadic cases of CCPP are also being reported from many more countries [37]. It mostly occurs in countries of Africa, Middle East and Asia.

#### **10.3 Transmission**

The disease is highly contagious and main mode of transmission is through inhalation of infected aerosols. The direct contact with affected animals is the main source of transmission. Airborne transmission can result in distant spread of about 50 m distance. However, the shorter survival time (3–14 days) of the organisms in external environment limits transmission of Mccp [38]. Yet under cold, moist and overcrowded environment these bacteria can persists for longer durations and may lead to severe outbreaks mostly in winter.

#### **10.4 Clinical signs**

CCPP is strictly a respiratory illness and is characterized by severe dyspnea, nasal discharge, cough, and fever. This can occur in peracute, acute and/or chronic forms in endemic areas. In peracute form, affected goats may die within 1–3 days without premonitory clinical signs. In acute infection, the initial signs are high fever (41–43°C), lethargy and anorexia, followed within 2–3 days by coughing and laboured breathing. The cough is frequent, violent and productive. In the final stages of infection, the goat may not be able to move and stands with its front legs wide apart and its neck stiff and extended [37]. Saliva can drip continuously from the mouth, and the animal may exhibit grunt or bleat in pain. Frothy nasal discharge and stringy saliva may be seen terminally. Pregnant goats may abort. Acutely affected goats generally die within seven to 10 days. In the chronic cases, there is chronic cough, nasal discharge and debilitation. These forms with resembling clinical signs in goats were also reported from captive wild goats.

Pathological features during necropsy are also limited to respiratory system. Acute form is characterized by unilateral pneumonia and sero-fibrinous pleuritis with straw colored fluid in the thorax. The lung is granular with copious straw-colored exudates oozing out on cut section. Pea-sized, yellow-colored nodules may be noticed in lungs and these nodules are surrounded by areas of congestion. Varying degrees of lung consolidation or necrosis may also be noticed [37]. The regional lymph nodes mainly bronchial lymph nodes are enlarged. Some long-term survivors reveal chronic pleuropneumoniae or chronic pleuritis, with encapsulation of acute lesions and numerous adhesions to the chest wall. The interlobular septa are not usually thickened in domesticated goats.

#### **10.5 Diagnosis**

CCPP can be diagnosed based on cultural, biochemical, serological, and molecular methods following a tentative clinical diagnosis. Ultrasonography and X-rays may help in diagnosis and CCPP-associated changes may be evident in lungs, pleura, thorax, and associated structures. Cultural isolation and identification ('fried egg-like appearance' of the colonies under microscope), though is conventional but is still considered as standard method for detection of Mccp from lung tissue and/or pleural fluid at necropsy. Due to the difficulty in isolation, PCR is the technique of choice for the diagnosis of CCPP. The agglutination tests, ELISA, FAT, CFT (most widely used), passive or indirect haemagglutination tests (IHT) are the immunological methods employed for diagnosis of CCPP [38]. Latex agglutination test is being increasingly used in diagnostic laboratories as a pen side test. It can used to test whole blood as well as serum.

#### **10.6 Treatment**

Tylosin is considered the drug of choice against Mccp. Further, oxytetracycline is also found effective when administered in early stages of infection. However, some infections are slow to resolve.

#### **10.7 Preventive measures**

In endemic areas, proper care should be taken while introducing new goats into the flock. Flock testing, slaughter, and on-site quarantine may be helpful in controlling the spread of disease. Vaccines available in some areas may help in prevention

of the disease. The commercially available CCPP vaccine containing inactivated Mccp suspended in saponin provides protection for over 1 year [37].

## **11. Dermatophilosis**

Dermatophilosis is a chronic, exudative and sometimes proliferative dermatitis occurs in domestic ruminants, wild animals and occasionally in human beings. Also known as Cutaneous streptothricosis, Strawberry foot rot or Lumpy wool.

### **11.1 Etiology**

Dermatophilosis is caused by *Dermatophilus congolensis*, which is a gram positive, nonacid-fast, facultative anaerobic actinomycete that produces motile zoospores.

### **11.2 Epizootiology**

The disease occurs worldwide and is more common in tropics and subtropics. The organism is believed to be a saprophyte of soil and persists in dry scabs and crusts, to survive for up to 42 months. It has been reported from many countries, but occurs particularly in humid climates and areas where ticks of the genus *Amblyomma* are endemic [39].

### **11.3 Transmission**

Transmission occurs by direct contact with infected animals. The infection can be transmitted indirectly by mechanical vectors (ectoparasites) and also through intradermal inoculation by contaminated thorny bushes. The pathogenesis may be influenced by factors such as mechanical injury to the skin, rainfall, tick infestation, concurrent diseases and/or stresses that compromise the host's immune system.

### **11.4 Clinical signs**

The disease is painful but non-pruritic, and is characterized by exudative, proliferative or hyperkeratotic dermatitis, accompanied by the production of crusts and folliculitis. In sheep, it may be seen in two forms: mycotic dermatitis (lumpy wool) and strawberry foot rot. While in goats and cattle, similar signs of crusty, suppurative dermatitis are seen and are often referred as cutaneous streptothricoses. The skin lesions appear raised, thick, yellow-brown colored discrete or confluents crusts containing matted hair. Sometimes may be seen in nodular form also with discrete encrustation of scab. The whole body may be affected but less hairy parts such as ears, axilla, scrotum, prepuce, ventral abdomen, limbs etc., show severe lesions [40]. Lesions in younger goats are mostly seen along the tips of the ears and under the tail. Most affected animals will recover within 3–4 weeks and lesions have little effect on overall health. In severe generalized infections, the animals often loose condition. If there are lesions at the feet, lips and muzzle, the movement of animals and eating become difficult.

### **11.5 Diagnosis**

Diagnosis of dermatophilosis is mainly based clinical signs particularly based on the appearance of the characteristic skin lesions. The same can be confirmed

by the demonstration of the organism from the lesions beneath the scabs. The softened scab materials stained by the Giemsa method, reveal the characteristic branching filaments containing zoospores. The organism can be cultured on blood agar at 37°C under 2.5–10% CO2 for up to 5 days and Haalstra technique based on chemotaxis of the zoospores to CO2 can be employed for efficient recovery of the organism.

### **11.6 Treatment**

Animals can be treated with antibiotics such as high doses of penicillin or long acting tetracyclines. Topical applications alone are ineffective. Antibiotic therapy is augmented by topical treatment with lime sulfur as well as control of ectoparasites and biting flies. Povidone iodine shampoos or chlorhexidine solutions also help in clearing the disease.

### **11.7 Preventive measures**

Control measures are based on minimizing the effects of predisposing factors and prompt treatment of affected goats. Animals with skin lesions must be isolated and treated at the earliest. Minimizing moist conditions (such as providing shelter during rainfall) is helpful in control and prevention. Grazing management especially removal of thorny bushes in pasture land that damages skin will also help. Prophylactic antibiotic therapy can also be given.

### **11.8 Public health significance**

*D. congolensis* is a zoonotic organism and rare human infections have occurred from handling diseased animals.

### **12. Foot rot**

A contagious, either acute or chronic dermatitis of the hoof and its underlying tissues leading to lameness [41].

### **12.1 Etiology**

Foot rot is caused by *Dichelobacter nodosus* and *Fusobacterium necrophorum*, anaerobic, non-spore forming, gram negative rods.

### **12.2 Epizootiology**

The organism *F. necrophorum* is ubiquitous in nature while *D. nodosus* is obligate pathogen, can be present in skin and hoof of animals and cannot survive much longer in environment. Moist environment, humid condition, wet grounds and overcrowding are the predisposing factors for foot rot [42].

### **12.3 Clinical signs**

Interdigital region will be moist and will have a foul odor due to necrosis (**Figure 8**). Lameness is the common sign of foot rot. Based on the severity of the infection animals may lose weight due to anorexia and there will be decrease in production [43].

#### **Figure 8.**

*Moist, necrotic interdigital region seen in foot rot condition. This figure is propriety of the authors.*

### **12.4 Diagnosis**

Diagnosis is based on clinical signs and isolation of organism from the foot lesions. Since the organisms are anaerobic isolation is tricky and hence molecular diagnosis like PCR can be used for diagnosis.

### **12.5 Treatment**

Hooves of the animals should be trimmed so as to remove the necrotic material thereby eliminating the anaerobic environment. Local antibiotics may be applied to the affected hoof after trimming. 10% zinc or copper sulfate or 10% formalin can be used for footbath [44].

### **12.6 Preventive measures**

*D. nodosus*, though present in epidermal tissues of the hoof, survives for less than 7 days in the environment and hence, affected animals should be separated from the herd to prevent spread to other animals. Regular hoof trimming and cleaning should be practiced. Bacterins can be used as vaccines to prevent the infection.

### **13. Conclusions**

Goat is called as poor man's cow but there are various bacterial diseases that cause economic loss to the goat farmers. Serval bacterial diseases cause acute infection hence there will be sudden onset of infection leading to huge mortality. Measures like use of vaccines before onset of disease, good management practices, etc., are essential to prevent the disease outbreaks. Animals with infection or clinical signs should be separated from rest of the animals so that infectious pathogens do not transmit to naïve animals and it is also recommended to quarantine newly purchased animals before admitting them into the farm. These practices can curtail the spread of infectious agents. It is also advisable to screen for diseases before purchasing the animals to the farm. Diseases like TB, JD and brucellosis should be screened before the purchase since these diseases are chronic in nature hence can remain undiagnosed. Animals infected with diseases that can affect human like anthrax, brucellosis, etc., should be handled carefully and better bio-security measures should be followed to prevent spread of disease within herd and also to human beings. Most of the bacterial infection can be treated with antimicrobial agents but these agents should be used judiciously because in the recent times antimicrobial resistance is a major problem.

## **Conflict of interest**

The authors declare no conflict of interest.

### **Author details**

Kumaragurubaran Karthik\* and Manimuthu Prabhu Tamil Nadu Veterinary and Animal Sciences University, Chennai, Tamil Nadu, India

\*Address all correspondence to: karthik\_2bvsc@yahoo.co.in

© 2021 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

*Bacterial Diseases of Goat and Its Preventive Measures DOI: http://dx.doi.org/10.5772/intechopen.97434*

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### **Chapter 14**

## Management and Control of *Eimeria* Infection in Goats

*Saw Bawm and Lat Lat Htun*

### **Abstract**

Coccidian parasites of the genus *Eimeira* cause coccidiosis in farm animals, which develop in both the small and the large intestines. Coccidiosis is a major economic concern in many livestock, especially in young animals, as a result of losses caused by clinical infection (diarrhea) and subclinical (poor weight gain in particular) and the required treatment costs. Herein, we summarize geographical distribution of *Eimeria* parasites, their life cycle, pathogenesis, clinical signs, economic losses due to coccidiosis, diagnosis, recent information on control and prevention, and anticoccidial drugs for *Eimeria* infection in goats. With regard to poverty alleviation in most developing agricultural countries, it is important to maintain and develop goat-related industries. Proper management should be used to prevent losses and reduce the productivity from coccidiosis in young animals by: reducing the level of environmental contamination by infectious oocysts; minimizing stress; and avoiding overcrowding.

**Keywords:** *Eimeria* infection, goats, management, control, anticoccidial drugs

### **1. Introduction**

The world populations of 2.3 billion small ruminants (goat and sheep) which comprise 1.09 billion goats [1] provide vital milk, meat and fiber. Goats (and sheep) are particularly important in Asia and Africa where they account for more than 90% and nearly 70% respectively of the world stocks [2]. Coccidian parasites of the genus *Eimeria* cause coccidiosis in small ruminants, which develop in both the small and the large intestines and specifically affect young animals [3]. In many livestock, especially in young animals, coccidiosis is of great economic importance as a result of losses due to clinical infection (diarrhea) and subclinical (poor weight gain in particular) and the required treatment costs. In goats, the majority of *Eimeria* infections are asymptomatic; notwithstanding, a few species have been linked to diarrhea and hindered growth [3, 4]. The coccidian are intracellular parasites, members of the protistan phylum Apicomplexa, subclass Coccidiasina. The genus *Eimeria* and *Isospora* are homoxenous, they develop both sexually and asexually in the same host [5]. Various *Eimeria* spp. are known to be involved in different ruminant hosts (bovine, ovine, caprine), however, because of the strict specificity of the host, no cross infection take place [3]. The *Eimeria* species do not transmit from animal species to another.

Studies in some countries such as Sri Lanka [6], Iraq [7], Jordan [8], Austria [9], Turkey [10], Saudi Arabia [11], China [12], Brazil [13] and Iran [14, 15] have shown that coccidiosis in goats is an important clinical and subclinical disease that may be linked to serious economic losses, especially under intensive breeding conditions with high animal density and high productivity [16]. Of the 16 *Eimeria* species

identified in goats worldwide, *E. arloingi, E. ninakohlyakimovae, E. christenseni*, and *E. caprina* were considered being the most pathogenic species [17–20]. According to reports [3, 21], the common species of *Eimeria* in goats are listed in **Table 1**.

### **1.1 Geographical distribution**

In temperate areas including Europe, *E. ninakohlyakimovae*, *E. arloingi, E. christenseni, E. jolchijevi, E. alijevi, E. caprina and E. caprovina* are the most prevalent *Eimeria* species in goats [22]. In semi-arid zones (Gran Canaria, Spain), the most common *Eimeria* spp. are *E. ninakohlyakimovae, E. arloingi* and *E. alijevi* [4]. In USA (mid-western states), *E. arloingi* (98.8%), *E. christenseni* (58.2%), *E. ninakohlyakimovae* and *E. parva* (33.3%) are the most frequent *Eimeria* spp. found in goats [23]. In dry tropical areas such as Senegal, the common coccidia species are *E. arloingi* (64%) and *E. ninakohlyakimovae* (56%) [24]. Similar findings have been reported in Ghana [25], Nigeria [26], Kenya [27, 28] and Zimbabwe [29]. In dry areas of Sri Lanka, *E. ninakohlyakimovae* (31%) *E. alijevi* (29%) and *E. arloingi* (21%) are the three most prevalent coccidia [6]. In Myanmar, the most common species of *Eimeria* found in goats are *E. arloingi* (25.4%), followed by *E. hirci* (20.7%) and *E. christenseni* (13.9%) [30]. High prevalence of *Eimeria* species infections, *E. arloingi* (64–80%) and *E. christenseni* (60%), have been reported in dry tropical areas of Africa (Senegal) [24], Nigeria [26], and Zimbabwe [29]. The occurrence of mixedspecies infection was higher than single-species infection [12, 26, 31]. Coccidia of small ruminants, therefore, exist globally, and it appears difficult to say that there is any specific geographical distribution for one or the other species of coccidia.

### **1.2 Life cycle**


*Eimeria* usually needs only one host in which to complete their life cycle. Within a host's intestinal cells, two stages, schizogony/merogony and gamogony grow up.

#### **Table 1.**

*Common species of* Eimeria *in goats.*

*Management and Control of* Eimeria *Infection in Goats DOI: http://dx.doi.org/10.5772/intechopen.98979*

Sporogony/sporulation, on the other hand, takes place outside of the host within an oocyst protecting infectious sporozoites. The life cycle involves an extracellular oocyst maturation stage (sporogony) as well as a parasitic intracellular stage inside the host with a sexual reproduction accompanied by an asexual [16].

When the unsporulated oocysts pass through the feces, after 2–7 days they become infected depends on *Eimeria* species and environment. The first single cell is divided into four sporoblasts, each of which grows into single sporocyst with two sporozoites [32]. The sporulated oocysts are resistant to adverse environmental conditions. They are able to live for several months or even over a year. Extreme desiccation, direct exposure to the sunlight, however, limits the survival of the oocysts, and temperatures below −30°C or above 63°C are lethal for the oocysts. The oocyst has thick-wall and usually ovoid form [16].

After ingestion by the host, the walls of the oocyst break down, releasing sporozoites from the sporocysts. The sporozoites penetrate the small intestine through an epithelial cell and develop into schizont of the first generation. The schizonts release motile merozoites, which may either initiate a second generation of schizonts or develop into gamont, gametes and then non-sporulated oocysts, which are released with the feces. The schizogony of second generation in the large intestines usually occurs with another generation of merozoites invades epithelial cells and develops the sexual stages, the gametocytes, male (microgametocytes) and female (macrogametocytes). Second-generation schizogony and fertilization of the gametocytes (gametogony) cause functional and systemic lesions of the large intestine [16]. In general, prepatent period for *Eimeria* species in goats is approximately 19 days [33]; however, the prepatent period is 20 days, 14–23 days, 10–13 days and 17–20 days for *E. arloingi*, *E. christenseni*, *E. ninakohlyakimovae* and *E. capria*, respectively [34]. Life cycle of *Eimeria* spp. in goat is shown in **Figure 1**.

#### **1.3 Pathogenesis and pathology**

The pathological and clinical outcomes are influenced by a number of factors such as the present *Eimeria* species, infection dose, its replication potential, inflammatory immune and concurrent infections by other pathogens as well as management and related stress. Due to the intracellular localization of all internal

**Figure 1.**

*Life cycle of* Eimeria *species in goat. This figure was redrawn based on the picture in Taylor et al. [21].*

developmental stages, significant damage to the intestinal mucosa occurs. The outcome of *Eimeria* infections can vary greatly by parasite species as well as by individual host animal and farm. The damage caused by the parasite infection and replication occurs most during the late schizogony and gamogony [35]. This is due to the multiplication that the parasite undergoes during its first schizogony, leading to an exponential increase in the number of intestinal cells during subsequent multiplication. As a result, most of the damage occurs shortly before oocyst excretion starts in affected animals.

In early infections with *E. ninakohlyakimovae* or *E. caprina* in goat kids are characterized by haemorrhagic enteritis [36]. Polyps in the small intestine may develop as a result of *E. arloingi* infections [18], and *E. apsheronica* induce formation of white nodules in the mucosa that are visible from the serosal surface [37].

#### **1.4 Clinical signs**

*Eimeria ninakohlyakimovae* and *E. caprina* are highly pathogenic species capable of inducing watery to bloody diarrhea [13]. The infections with *E. arloingi* can also lead to watery diarrhea [38]. Acute symptoms may not exist in older animals at all or only in a small numbers of the affected goats following reinfection. Subclinical coccidiosis following infection with pathogenic species can be expected to produce subacute to chronically adverse impacts on the health, feed efficiency, and prolonged productivity [28]. Coccidia can invade and kill hosts' intestinal cells that cause anemia, loss of electrolyte and poor absorption of nutrients.

Most affected goats show diarrhea, poor growth rate, weakness and rough hair coat [12]. The feces are soft, watery and have clumps of mucus and color shifts from brown to yellow or dark tarry [18]. Loss of weight and dehydration are noted. Because the appetite is decreased, the animals' general condition is worsened. In some cases, sudden deaths occur in young animals between 2 and 4 months old without preceding digestive signs [3]. Diarrhea with or without mucus or blood, dehydration, emaciation, fatigue, and death are common clinical signs. But in fact, some goats are constipated and die acutely without diarrhea.

Impairment of growth is the major sign in subclinical form of coccidiosis. Early signs in acute cases include decreased appetite, listlessness, fatigue and abdominal pain which can be manifested by crying and repeated rising up and lying down. First, the feces may be unpelleted, then pasty, and eventually watery yellowishgreen or brown diarrhea. The typical characteristics associated with coccidiosis are diarrhea that may be mucoid or bloody, abdominal pain, tenesmus, loss of appetite, fatigue, weight loss, rough hair coat, dehydration and anemia. Fever, ocular and nasal discharges can occur in the acute disease. Clinical coccidiosis is common in lambs 4–6 weeks old. Acute, bloody diarrhea can occur in severe cases, as a result of extensive damage to the intestinal epithelium [39].

While coccidiosis is self-limiting, the clinical presentation can be exacerbated further by other enteric pathogens. Exposure to low-grade challenges results in development of a strong immunity against to the disease. Successive infections in young animals might lead to the excretion of a large numbers of oocysts in animals, which leads to heavy contamination of houses, pastures or watering places [34].

#### **2. Materials and methods**

The present chapter intends to give a comprehensive approach of the importance of *Eimeria* parasite in goats, pathogenesis, clinical signs, diagnosis and economic losses due to coccidiosis. In addition, this chapter aims to explore the

recent information on control and prevention, and anticoccidial drugs for *Eimeria* infection in goats. The databases were searched from PubMed and Google Scholar search. Search terms were "*Eimeria* in goats" and "coccidiosis in goats". A total of 130 articles were retrieved from the search. These studies were conduct in different regions of the world with different breeds of goats. Findings of anticoccidial studies carried out in the author's laboratory were also included.

### **3. Economic impact**

Some assumed parameters for estimation of economic losses are summarized in **Table 2**. There are not well documented economic impacts of coccidiosis in small ruminants and no published data for economic losses due to subclinical or clinical disease in tropical regions are available. While subclinical coccidiosis might not be of great importance, it cannot be compared to other infections [5]. Where the high density of animals with high productivity can cause coccidiosis to become an infection of great economic significance in small ruminants [16]. In the case of a mild infection, these losses can be attributed to reduce productivity with no clinical signs.

Global sheep and goats production was being estimated to lose up to \$140 million per year [40]. Losses result from mortality, treatment costs for animals with diarrhea, enhanced sensitivity to secondary infections in infected animals, and reduced production efficiency. Beside the acute impacts, a prolonged effect was suggested as regards a lower feed efficiency, less final growth performance, and a reduced reproductive performance for life [41]. Subclinical coccidiosis is believed to cause higher production losses than clinical coccidiosis, since animals are infected and are affected for long-term [42].


**Table 2.**

*Assumed parameters for estimation of economic losses due to coccidiosis in goats.*

### **4. Diagnosis**

There are different diagnostic methods available for specific identification of *Eimeria*. They are based mainly on clinical observations. The most direct, definitive, and cost-effective method of diagnosis continues to be the microscopic examination of diarrhoeal or bloody feces from young animals [42]. Traditional methods are primarily based upon microscopic oocysts morphological features, parasite biology, clinical signs in animals affected, and typical macroscopic lesions assessed by lesion scores [44]. In general, fecal samples are collected and analyzed

**Figure 2.**

*Oocysts of* E. christenseni *(A),* E. arloingi *(B) and* E. hirci *(C) from goats in Myanmar identified by Bawm et al. [30].*

for the presence of *Eimeria* oocysts (**Figure 2**). Fecal flotation enables oocysts to concentrate and increases their sensitivity significantly. Moreover, species-level identification should be performed. As many of the *Eimeria* species are either not or mildly pathogenic, it is possible to determine whether the *Eimeria* oocysts found are associated with a clinical disease or only an accidental finding and whether the cause of this disease requires more study. Pooled fecal samples can be used for monitoring purposes, while clinically ill should be individually sampled so that the excreted amount of *Eimeria* oocysts can be easily estimated. Accurate quantification of oocyst excretion in individual samples from animals in the focus groups can be helpful. There are several quantitative flotation methods available, with the McMaster counting technique being the most common method one [8].

However, the morphological approach is not entirely accurate due to the prevalence of intraspecies heterogeneity, as natural *Eimeria* infections are typically mixed with more than one species and some species have confounding characteristics [43, 44]. In addition, morphological observations are very labour-intensive in conjunction with fecal analysis and require a professional method of classification. In order to overcome the limitations of conventional methods [45–47], molecular techniques have been identified as useful for species identification or classification of this genus and have further demonstrated the phylogenetic location of each *Eimeria* species and phylogenetic clades [48, 49]. Molecular characterization of *Eimeria* goat species has been recorded in Australia [50], India [51], Iran [52] and Myanmar [30].

#### **5. Prevention and control**

Coccidiosis in ruminant is usually controlled by a combination of good management and treatment with anticoccidial drugs or prophylactics [42]. In general, effective control of coccidiosis is not based on the complete removal of *Eimeria* from the affected premises. It is considered neither possible nor useful to avoid contact between the naïve hosts and *Eimeria* for the operation of this parasite. Low-dose infections are generally not linked to disease, and low-dose infections are beneficial to the host because they allow the host to develop a protective, non-sterile immunity and protect against future infections. Therefore, instead of pathogen eradication, the emphasis of ruminant coccidiosis management lies in reducing the infection burden to uncritical levels and endemic stability [42].

Prevention is mainly based on the management of herds, including hygienic measures, since no vaccine is available. Coccidiosis outbreaks are a herd-level problem that is driven by stress. Infected animals need a responsive immune system to prevent severe disease. Therefore, minimizing or eliminating stressors like diet changes, harsh climate conditions, crowding, frequent shipping, animal grouping and exposure to other disease pathogens is a crucial part in preventing disease [16]. It is important to ensure adequate nutrition and appropriate uses of anticoccidial drugs. Colostrum uptake is important for newborn ruminants as it protects them from pathogens. Although the protection against *Eimeria* is not efficient, the protection from other pathogens supports and prevents problems in the animals' immune system.

Proper hygiene and minimizing predisposing factors in the environment are important for the control strategies of coccidiosis [53]. Pens for lambing and kidding should be kept clean, and bedding should be disposed when old or infested with oocysts. The washing and disinfecting of the buildings must be done with boiling water under pressure and gaseous ammonia [54].

All steps that minimize the amount of fecal contamination on hair coats should be routinely applied. Feed and water troughs should be high sufficient to prevent heavy fecal contamination. Feeding animals on the ground should be avoided, particularly when overcrowding. The regular rotation of pastures for parasite control will also assist in the controls of coccidial infection [53].

### **6. Anticoccidial drugs**

With respect to available anticoccidials, they are usually supplied as feed additives, in drinking water, or in feed supplements such as salt. As a result, their use is often most feasible in weaned animals. However, anticoccidial prevention may need to start in the first weeks of life depending on the procedure [3]. In general, coccidiostats and coccidiocidal drugs are available. The development of internal coccidia stages is inhibited by coccidiostats, while coccidiocidal drugs kill the parasites. Drugs of both modes of action are currently available on the market. The best time to administer a prophylactic treatment would allow for the infection to develop but not for full parasite development. An appropriate treatment given following or prior to infection by the onset of oocyst release and appearance of symptoms is known as metaphylaxis. Anticoccidial therapy would therefore be optimally applied after infection, for the most important ruminant *Eimeria* species, approximately 14 days after infection, when the first and second merogonies develop. The main advantage of metaphylaxis over prophylaxis is the development of immunity and protection against reinfection, which is unlikely to make any subsequent anticoccidial treatments necessary. In general, it is important to apply prophylactic and metaphylactic treatment on the basis of a herd or animal group, as infected animals cannot be determined and all animals living in the same contaminated environment would be exposed to *Eimeria* infections. Continued use of coccidiostats reduces the number of oocysts passed through the feces over time, but may also lead to selection for resistance and therefore a regular monitoring of the treated animals is needed [16].

Anticoccidial drugs belong to one of two categories [55, 56, 63]:

	- a.Monovalent ionophores (monensin, narasin, salinomycin)

b.Monovalent glycosidic ionophores (maduramicin, semduramicin)

	- a.Inhibition of parasite mitochondrial respiration (decoquinate, clopidol)
	- b.Inhibition of the folic acid pathway (sulfonamides)
	- c.Competitive inhibition of thiamine uptake (amprolium)
	- d.Inhibition of respiratory chain enzymes and nuclear division of protozoan (e.g., diclazuril, halofuginone, nicarbazin, robenidine)

Polyether ionophores inhibit the growth of sporozoites by increasing the concentration of intracellular Na<sup>+</sup> ions. They also accelerate the activity of Na+/K+/ ATPase [57] and affect merozoites by inducing the breakup of the cell membrane [58]. Monensin was the first antibiotic to show an anticoccidial effect at reasonable concentrations, allowing it to be used in feed [59]. It can act as an effective anticoccidial agent for coccidiosis caused by *E. crandallis*, *E*. *christenseni* and *E*. *ninakohlyakimovae* in goats kept in confined space [60].

Monensin fed prophylactically at 20 g per ton of feed for 28 days decreases shedding of oocysts and improves feed conversion. However, high monensin levels make the feed unpalatable and toxic [53, 60]. It is believed that toxic effects in the horse, cattle, dogs, cats, rats, avian species and goat are mediated by interference with cell membranes ion gradients, inducing mitochondrial disruption and thus depleting of cellular energy [61, 62]. The documented toxic effects include heart toxicity, muscle degeneration and neuropathy, the latter is shown by myelin and ataxia [62].

Quinolones, pyridones, alkaloids, guanidines, thiamine analogues, and triazine derivatives are examples of synthetic anticoccidial drugs. Triazines inhibit nuclear division of protozoan thus interfere with the development of schizonts and gametocytes [63]. Decoquinate (0.5 mg/kg BW) and lasalocid at a dose of 25-100 mg/kg feed can be used to treat coccidiosis from weaning to market [53]. Sulfonamides at dosage rates of 25 to 35 mg/kg BW for at least 15 days are effective against coccidiosis in small ruminants. The combination of chlortetracycline and sulfonamide has provided protection in lambs. Other drugs include monensin (20 and 16 g/ton of feed for sheep and goats, respectively), toltrazuril (20 mg/kg BW as a single oral dose) and diclazuril (2 mg/kg BW as a double oral dose) [34, 53, 64].

Amprolium in feed is also used to treat the disease in goats (100 mg/kg BW for 21 days) and sheep (50 mg/kg BW for 21 days) [53]. Amprolium is structurally related to thiamine, and it is believed to be associated with a competitive inhibition of successful transportation of thiamine into parasite [65]. The production of oocyst in lambs has proved to be decreased when given as an in-feed medicine and clinical coccidiosis outbreaks have been successfully controlled by single drenching [66]. Young *et al*. [65] also stated that reductions in oocyst production have been detected in goats.

Diclazuril and toltrazuril have shown in several studies to decrease production of oocysts in natural and artificial *Eimeria* infections when orally given to young cattle, pigs, or lambs prior to the onset of clinical signs [67–71]. The molecules of decoquinate, toltrazuril, and diclazuril act on the whole coccidial cycle and allows curative as well as preventive action [53, 72]. According to our recent study [73],

*Management and Control of* Eimeria *Infection in Goats DOI: http://dx.doi.org/10.5772/intechopen.98979*

among the treated group of goats with monensin, toltrazuril, and amprolium, the percentage reduction in the number of fecal oocyst in the toltrazuril- treated group was found to be observed the highest (92%).

Resistant problems have been reported for some anticoccidial drugs, such as arprinocid and quinolone buquinolate [74]. In the field trials, toltrazuril resistance did not exist in at least five consecutive drug exposures [75]. The polyether ionophores became the drug of choice in 1972 and, as of today, are now the most commonly used drugs in poultry. Although ionophores resistance is likely to develop slowly due to their specific mode of action, resistance development in synthetic drugs with a specific mode of action appears to be faster, involving genetic mechanisms [76].

### **7. Conclusion**

In this review, we highlight the management and control of *Eimeria* parasite in goats, the causative agent of coccidiosis, which is of great economic importance as a result of losses due to clinical diseases (diarrhea) and subclinical (poor weight gain) and the required treatment costs. We summarize the geographical distribution of *Eimeria* parasites, their life cycle, pathogenesis, clinical signs, economic losses due to coccidiosis, diagnosis, recent information on control and prevention, and anticoccidial drugs for *Eimeria* infection in goats. With regard to poverty alleviation in most developing agricultural countries, it is important to maintain and develop goatrelated industries. Proper management should be used to prevent losses and reduced productivity from coccidiosis in young animals by reducing the level of environmental contamination by infectious oocysts, minimizing stress, and avoiding overcrowding [3]. It is essential to be aware of the problem and to implement control strategies, such as the maintenance of hygienic conditions and use of anticoccidial drugs.

### **Conflict of interest**

The authors declare no conflict of interest.

### **Author details**

Saw Bawm1 \* and Lat Lat Htun2

1 Department of International Relations and Information Technology, University of Veterinary Science, Nay Pyi Taw, Myanmar

2 Department of Pharmacology and Parasitology, University of Veterinary Science, Nay Pyi Taw, Myanmar

\*Address all correspondence to: bestshadow@gmail.com; sawvet@uvsyezin.ed.mm

© 2021 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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### **Chapter 15**
