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COLIBACILLOSIS

This is a disease of new-born lambs and kids caused by pathogenic strains of Escherichia coli and characterised by septicaemia or enteritis depending on the strains of bacteria involved.

Epidemiology

The disease is common under intensive production systems. Faeces of infected animals are the main sources of infection. Sub-clinically infected animals act as reservoirs which contaminate bedding, pens and feed or water troughs making them sources of infection. People working with animals can transmit the infection between herds or pens. Stress factors such as cold, wet or windy weather; poor hygiene in animal houses and overcrowding predispose animals to the disease. Inadequate intake of immunoglobulins
through colostrum immediately after birth has also been found to increase the susceptibility of animals to the septicaemic form of the disease (colisepticaemia). Outbreaks may occur when there is mass lambing or kidding. The losses associated with colibacillosis in small ruminants in sub-Saharan Africa are not well documented. This may probably be because, with the exception of small ruminant intensive production units in few countries such as South Africa, Kenya and Zimbabwe the majority of sheep and goats in the region are kept extensively and hence, the incidence of the disease is low. However, with increasing population pressure and decreasing land available for grazing, intensive small ruminant production systems are being adopted especially in urban or peri-urban areas. This change of management systems may be associated with an increase in incidence of the disease.

Pathogenesis

The occurrence of clinical colibacillosis depends on the type and pathogenicity of the infecting strain of E. coli, host susceptibility and presence or absence of predisposing factors. Thus, two syndromes of the disease, that is, septicaemic (colisepticaemia) and enteric colibacillosis can occur. Colisepticaemia is caused by invasive strains of E. coli. Invasion of tissues may occur through the intestinal lumen, the umbilical vessels, nasopharyngeal mucosa and tonsillar crypts. Posses adhesive pili, resistance to antibacterial activity of serum and production of endotoxin are the factors which enhance the
pathogenicity of the invasive strains of E. coli. Presence of receptors for the pili in the epithelium of intestinal mucosa also facilitates establishment of the bacteria. After successful establishment on the mucosa the bacteria produce endotoxins which pass into systemic circulation and initiate bronchoconstriction, pulmonary hypertension and pulmonary oedema. Invasive bacteria also cause
tissue damage. Enteric colibacillosis is caused by enterotoxigenic strains of E. coli which are
capable to colonise, proliferate and producing an enterotoxin in the upper small intestine. The bacterial fimbriae attach on the receptor sites on the villous epithelial cells and the bacteria multiply and colonise the villous surface. The colonisation of the villi and production of enterotoxins disrupt the absorptive
mechanisms on the intestinal surface resulting in the secretion of fluids and 53 electrolytes from the systemic circulation into the intestinal lumen. This leads to electrolyte imbalance, dehydration, acidosis, hyperkalemia, circulatory failure and death.

Clinical and pathological features

Septicaemic colibacillosis is common in lambs and kids. Lambs and kids of 1-2 days and 3-8 weeks old have been found to be the most susceptible groups. The syndrome may be peracute in which case sudden death occurs without any premonitory signs. The acute disease is characterised by stiff gait or recumbency, depression, fever, hyperaesthesia and tetanic convulsions. Animals may collapse because of acute meningitis. The chronic form of the disease is characterised by polyarthritis. The bacteria may also cause local reactions in other tissues. No gross pathological lesions are observed in peracute septicaemic colibacillosis because of sudden death. In the acute form there are widespread subserosal and submucosal petechial haemorrhages. Enteritis and gastritis are common features.
Fibrinous exudates are found in joints and in serous cavities. Fibrinopurulent meningitis and peritonitis may also be encountered. Infection through the umbilicus is associated with omphalophlebitis.


Enteric colibacillosis is manifested mainly by a haemorrhagic or mucoid diarrhea various degrees of diarrhoea and slight fever. Other enteropathogens such as rotaviruses, salmonellae and Campylobacter spp may also be involved and complicate the clinical picture. Pathologically there are widespread haemorrhages in the intestinal mucosa and large numbers of the bacteria can be demonstrated in smears from the intestinal mucosa.

Diagnosis

The epidemiology, clinical signs, pathological features and, response to treatment may support a presumptive diagnosis of colibacillosis. Confirmation is achieved by the isolation and characterisation of E. coli from suspected animals. Bacterial culture alone is of limited use because of the presence of non-pathogenic strains of E.coli and, demonstration of specific toxins may be of great value to support the diagnosis. In the peracute form of the disease the organisms may be isolated from abdominal viscera and
heart blood. The differential diagnosis of colisepticaemia include clostridial enterotoxaemia and
salmonellosis. These conditions can be confirmed by isolation and identification of the causative bacteria. The differential diagnosis of enteric colibacillosis include dietetic diarrhoea, coccidiosis and campylobacteriosis. Dietetic diarrhoea is manifested by passage of voluminous and pasty or gelatinous faeces and the animals are usually bright or alert although they may be inappetent. Other enteritides can be differentiated by isolation and identification of their aetiologic agents

Treatment and Control

In view of the diversity of strains of E. coli which are involved in the syndrome it is important to carry out drug sensitivity testing before any treatment is instituted. Trimethoprim-sulphonamide combination (15-25 mg/kg) and kanamycin (20 mg/kg) given parenterally and colistin administered at a rate of 1-2 g/kg in drinking water have been found to be effective in the treatment of the disease. Other antibiotics such as oxytetracycline, neomycin, chloramphenicol and sulphadimidine are also used.
Vaccination of dams 2-4 weeks before parturition to stimulate production of specific antibodies is recommended in order to provide passive protection bf neonatal lambs and kids through colostral immunoglobulins. Formalin-killed whole-cell vaccines are commercially available. Specific E. coli strain vaccines produced using K99+ pili antigens have been found to confer immunity to lambs and kids. Ewes have to be vaccinated twice in their first year of lambing, first at 8-10 weeks and then at 2-4 weeks before lambing. In subsequent years, one vaccination 2-4 weeks before parturition has been found to be satisfactory. Maintenance of good hygiene in the animal environment can reduce
transmission and incidence of the disease. Provision of adequate colostrum to newly born kids and lambs will help to protect them from colisepticaemia.

SALMONELLOSIS

This is a disease of animals and man caused by different species of salmonellae and is characterised clinically by three major syndromes: peracute septicaemia, acute enteritis or chronic enteritis. Salmonella dublin, S. typhimurium and S. anatum are the common species associated with the disease in sheep and goats. S. abortusovis has been found to cause abortion in sheep.

Epidemiology

Salmonellae are widespread and the disease occurs world-wide. Salmonella spp are enteric bacteria and carrier animals shed the organisms in faeces thus contaminating the environment. It has been found that infection with S. dublin may result in a clinical disease or an active or passive carrier state. Active carriers constantly shed the organisms in faeces whereas, passive carrier will shed the organisms when stressed and, they may also manifest an overt disease. Recovered animals become subclinical carriers and shed the organisms in faeces. S. typhimurium may also originate from man or wild animals. Infection is acquired by ingestion of contaminated material. Animals may acquire the infection through food of animal
origin and pastures contaminated with infective slurry or improperly treated fertilisers. Watering points may be contaminated with slurry from infected herds or fertilisers. Intensification of animal management favours spread of the disease from carriers animals. The organisms may be introduced in the herd via contaminated feed stuffs, formites, birds or nematodes. Stresses such as transport, starvation, parturition, overcrowding in communal grazing land, holding yards and dips activate latent
infections and favour rapid spread of the disease. Disruption of the intestinal flora by factors such as antibiotic therapy, change of diet and water deprivation increases the susceptibility of the host to infection. Infection in animals occurs mainly by ingestion but in sheep it has been shown that infection may also be acquired by inhalation of infective material. Animal salmonellosis is the principal reservoir for human 55 salmonellosis.


Pathogenesis
The ability of Salmonella spp to produce disease is facilitated by the presence of virulence factors. It has been found that pathogenic salmonellae posses adhesive pili, protective plasmids and, produce an enterotoxin, cytotoxin and lipopolysaccharide. These act together and enable the bacteria to adhere and
colonise the intestinal epithelium, survive the phagocytic activity of macrophages and increase the permeability of the intestinal epithelium. The presence of bacteria on the intestinal wall also initiates an inflammatory response. After successful establishment, colonisation and disruption of the integrity of the intestinal wall, the organisms the pass through lymphatic system to mesenteric lymph nodes after which a clinical disease may occur depending on the virulence of the organisms, immune status and age of the host and, presence of intercurrent infections or other stress factors. From the mesenteric lymph nodes, the organisms invade the reticuloendothelial cells and then enter the blood stream causing septicaemia, enteritis and localisation in various tissues. Invasion of bacteria in the uterus and placenta causes abortion.

Clinical features

Enteric salmonellosis is the commonest form of the syndrome encountered in sheep and goats. The incubation period is 1-4 weeks. The syndrome is characterised by fever (40-41C), anorexia, listlessness, severe diarrhoea and sometimes dysentery or tenesmus. Faeces have a putrid smell, mucoid and may contain blood clots or fibrin casts. Fibrin sheets may be found in the intestinal mucosa. Shallow and fast
respiration, rapid pulse and congestion of the mucosae are observed. Abortion is a common feature. There may also be dehydration, toxaemia, loss of weight, prostration, recumbency and death. New-born animals that survive the septicaemic disease develop severe enteritis characterised by diarrhoea. Polyarthritis and pneumonia are a common sequel. Does and ewes often die after abortion and lambs
born alive may die subsequently. S. dublin is most common cause of the disease in goats. S. typhimurium also causes peracute septicaemia or acute enteritis.

Pathological features

Acute enteritis is characterised by muco-haemorrhagic enteritis and submucosal petechiation. In S. typhimurium infection, there is necrotic enteritis in the ileum and large intestines. The intestinal contents are putrid, mucoid, blood-tinged or may contain frank blood. The intestinal mucosa may be covered by an extensive diphtheritic membrane. The mesenteric lymph nodes are enlarged, oedematous and
haemorrhagic. There is also enlargement and fatty degeneration of the liver; thickening of the gall bladder wall and presence of blood-stained fluid in the serous cavities. The histopathological picture is characterised by necrosis, oedema, congestion and infiltration of the lamina propria and submucosa of the caecum, colon and small intestine with neutrophils, lymphocytes, plasma cells and macrophages. Focal necrosis in the mesenteric lymph nodes and thrombosis of the submucosa vessels
occur. Hepatocellular necrosis and neutrophilic and mononuclear cell infiltration in the portal tracts may be evident. Necrosis and neutrophilic infiltration in the 56 mesenteric lymph nodes and lymphoid and reticuloendothelial hyperplasia occur in protracted cases.

Diagnosis

A provisional diagnosis can be based on the epidemiological, clinical and pathological features and the disease can be confirmed by bacterial isolation and serotyping. In the acute disease the bacteria are present in heart blood, spleen, liver, bile, mesenteric lymph nodes and intestinal contents while in chronic cases, the bacteria can be isolated from the intestinal lesions or other viscera. Lymph nodes
which drain the caecum and lower intestine have been found to be rich in the bacteria. The organisms can be easily demonstrated in a thick smear made from the wall of the gall bladder. Selective media such as MacConkey agar, brilliant green agar, triple sugar iron agar and xylose-lysine deoxycholate medium are used in the isolation of Salmonella spp. Species-specific antibodies may be used to diagnose the disease but cross-reaction do occur. Coccidiosis, campylobacteriosis and parasitic gastroenteritis should be considered in the differential diagnosis of salmonellosis. Unlike the above conditions, salmonellosis is often manifested by a more acute and often fatal enteritis. High faecal oocyst and demonstration of developmental stages of Eimeria on the intestinal wall may be highly suggestive of coccidiosis whereas,
high faecal egg and worm burdens may be highly suggestive of parasitic gastroenteritis. These features are not observed in salmonellosis except when they occur as intercurrent infections. Campylobacteriosis can be differentiated by demonstration of Campylobacter spp in faeces.
Salmonellosis can be treated using chloramphenicol (20 mg/kg) infused intravenously at 6 hours interval for 3 days. Other drugs include trimethoprim-sulphadoxine combination, sulphadimidine, framomycin, ampicillin and amoxycillin. Oral nitrofurazone daily for 5 days mixed in the feed or as a drench is commonly used in mass medication during outbreaks. The recommended treatment regime is to combine oral and parenteral therapy. It is important to remember that oral antimicrobial therapy may disrupt the normal intestinal flora and increase host susceptibility to the disease. Supportive fluid therapy to alleviate the effects of dehydration and electrolyte loss is beneficial. In some countries, treatment of animals against salmonellosis has led to selection for drug resistant strains thus complicating the effectiveness of treatment of human cases of the disease. Salmonellosis can be controlled by avoiding faecal contamination of feed or water and maintaining good hygiene in the animal houses. Animals should be purchased from herds which are known to be free from the disease. Regular testing should be carried out to identify carriers which should be culled. Infected premises should be properly
disinfected and the infective materials should be destroyed. Personnel from infected herds should not be allowed to come into contact with disease- free animals. Vaccination of small ruminants against salmonellosis is not widely practised.


MASTITIS

Mastitis refers to the inflammation of the mammary gland and is characterized enlargement of the udder and abnormal milk secretion with or without fever. The disease has a multiple aetiology but Staphylococcus aureus and Streptococcus agalactiae are 57 the commonest bacteria isolated from cases of mastitis in small ruminants. Other bacteria encountered in include Corynebacterium pyogenes, Klebsiella spp, Mycobacterium spp and Brucella spp.

Epidemiology

Reports on clinical mastitis in small ruminants are available from South Africa, Kenya and Nigeria and, information from other countries is limited. This lack of information is probably be related to the fact that the indigenous small ruminants are kept primarily for meat and, hence little attention has been paid to the economic significance of mastitis. However, with recent introduction of dairy goats and intensification of management systems, mastitis may become an important disease entity worth attention. Un-hygienic conditions in animal houses and poor milking hygiene are important predisposing factors. Mechanical or surgical wounds in the teats or udder facilitate penetration of the bacteria. Most often, Mycobacterium spp and Brucella spp spread systemically and lodge in the mammary tissue causing mastitis.

Pathogenesis

After entry through the teat canal the bacteria colonise and multiply in the mammary tissue. Some bacteria produce enzymes and toxins which cause inflammation and damage to the mammary tissue, Pyogenic bacteria cause abscessation and suppuration. These inflammatory changes are associated with abnormalities in milk. The severity of infection is determined by the virulence of the organism, extent of mammary tissue damage, stage of lactation and efficiency of host defence mechanisms in the mammary
tissue.

Clinical features

The clinical signs of acute staphylococcal mastitis in goats include restlessness, elevated pulse (up to 144 per minute) and respiratory rate (up to 80 per minute) rates, hot, painful and enlarged mammary glands. Gangrenous necrosis of the mammary tissue may occur. On palpation there is marked diffuse induration of the mammary glands and enlargement of the supramammary lymph nodes. The milk
shows a thick yellowish discoloration or may be blood-stained.

Pathological features

The affected mammary glands are enlarged and hard on palpation. The teat orifices may be blocked. Abscesses may be present in different sections of the mammary tissue.

Diagnosis

A tentative diagnosis is based on the clinical signs especially presence of abnormalities in milk and pathological lesions. Confirmation is achieved by isolation or demonstration of the causative agents in smears prepared from pus or milk secretions. Cell counts and California mastitis test are also used in the diagnosis. Mastitis in goats' may also be caused by Mycoplasma agalactiae and Candida
albicans and these should be considered in the differential diagnosis of the disease. 58 Other mammary abnormalities such as oedema, passive congestion and haematomata are usually not associated with abnormalities in milk.


Treatment and Control
Bacterial mastitis can be treated by penicillin, streptomycin, oxytretracycline and
gentamycin either as intramammary infusions or parenterally in systemic cases.
Combination of systemic and intramammary antibiotic therapy is beneficial where there
is systemic involvement. Some strains of S. aureus are resistant to Penicillins, hence
drug sensitivity testing is recommended before the use of these drugs in the treatment
of mastitis. Proper herd and milking hygiene is the most effective means of controlling
mastitis.
Other bacteria such as Mycobacterium spp, Listeria spp, Actinobacillus spp
and Actinomyces spp cause disease syndromes in small ruminants, the clinical and
pathological features are similar to those observed in cattle








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