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NEONATAL DIARRHOEA COMPLEX

It is an acute disease of neonates characterized by diarrhoea, dehydration and death after a short course. In all diarrhoeas, the physiological result is the failure to absorb fluids or secretions that are increased into the intestine or both.

Aetiology


Diarrhoea is a clinical sign having multiple aetiological factors. For many years, Escherichia coli were considered as the primary pathogen in diarrhoeic Kids and the term colibacillosis has been in common use. Even now also it can cause the disease in Kids, piglets and lambs. However, the disease in Kids appears to be a disease complex with multifactorial aetiology and its interplay with environmental factors and managemental practices. Many bacteria, viruses, protozoa and fungi can cause diarrhoea in neonates.

Bacteria: E. coli is G-ve short rod, coccoid bipolar shaped to long filamentous form occurring in single or short chains. Usually these are motile with peritrichous flagella but some are non motile. This organism is incriminated as major cause of scours. Always the same serotype is not isolated from routine bacterial procedures. It is always present in the intestinal tract and can cause a secondary infection following viral agents. K-99 and K-88 are the common serotypes isolated from Kids and piglets. E. coli has been divided into 2 groups— enteropathogenic organisms and septicaemic groups. Enteropathogenic organisms are not invasive but localized in intestine especially in ileum and cause diarrhoea through the production of endotoxins. Commnonly 25% of the cases of Kids diarrhoea could be due to E. coli but it can reach up to 75%. The case fatality rate varies from 10-50%. Septicaenic serotypes have the ability to pass the intestinal wall and invade the tissue and these usually do not cause diarrhoea but localize in the brain and joints to produce meningo-encephalitis and arthritis, respectively. In Kids, the enteric from of colibacillosis is caused by enterotoxigenic strains of E. coli which are non-invasive and the septicaemic form is caused by the invasive strains of the bacteria. The most important enterotoxigenic strain involved in Kids is E. coli K 99+ which produces heat-stable enterotoxin. The site of predilection for these strains is the ileum of small intestine whereas the non-enterotoxigenic strains do not adhere to these sites. E. coli strains which commonly affect the piglets have several common features as that of the strains affecting the Kids like possession of K 99+ pilus and O antigen, production of heat-stable toxin, and formation of mucoid colonies. The enterotoxigenie strains of E. coli that cause intestinal fluid secretion in piglets have been classified into 2 classes depending upon the age group which they affect (a) class-2 affects piglets of less than 15 days of age. and (b) class-l cause fluid secretion in odder goats. Enteric colibacillosis is more common in goats, which are weaned from the sow immediately after birth and are reared on milk replacers. Enterotoxigenic E. coli have been isolated from the faeces as well as blood of lambs but these have not been characterized as in Kids and piglets.

Salmonella typhimurium and S. dublin commonly occur in 2-6 weeks old Kids. Clostridium perfringens type B and C are the most common producing a necrotizing toxin. Changes in managemental condition and weather might result in change in nursing habits of Kids that could result in overloading on milk, which may result in atony or hypomotility of digestive tract which is ideal for the growth of clostridial organisms and production of their toxins.

Viruses: Scours can occur within 12 hr after birth with an infection with reovirus. However when first introduced into a herd, Kids of one month or older may also be affected. Coronavirus causes scours in Kids of s days to 6 weeks of age. Parvovirus usually produces diarrhoea during the first week after birth. Bovine viral diarrhoea virus can cause diarrhoea in neonatal Kids and the Kids may become infected in utero or post-natally.

Protozoa: Coccidia affect young Kids of 3 weeks and above age. It can be a severe problem when overcrowding, poor sanitation and stress occurs. Eimeria bovis and E. zurnii are most predominant species isolated but others can also produce the disease. Cryptosporidia are intracellular protozoan parasites currently classified under sub-phylum sporozoa and sub-class coccidia. They occur in intestinal tract of mice, rabbits, guinea goats, dogs, cats, humans, Kids, reptiles and arthropods. Chlamydia psittaci is an obligate intracellular parasite of mucosal cells of abomasum and intestines. Fungi: Fungi like Candida, Mucor, Absidia, Aspergillus and Phycomycetes can come invasive and pathogenic following extensive antibiotic therapy.
Epidemiology

Colibacillosis is a common infectious disease encountered throughout the world causing neonatal diarrhoea in the farm animals and resulting in enormous economic losses due to increased mortality during the very early period of life. Though the newborn animals of less than 3 days of age are most susceptible, the disease may affect week-old animals causing mixed infection along with other enteropathogens. It may be attributed to the replncement of villous epithelial cells. which takes place during that period. The disease spreads primarily by ingestion of milk, water or feed contaminated by urine, faces or uterine discharge of infected animals; by consuming milk from udders of cows suffering from coli form mastitis, from the skin of soiled under or teat, contaminated bedding, etc. The infected but normal appearing Kids are the main reservoirs of the organism. The recovered Kids may shed the bacteria for up to several months. The portal of entry of the organism may be either through oral or umbilical vessels or naso-pharynx of the newborn.

Immune status or presence of immunoglobulin’s in the neonate’s plays an important role in the occurrence of disease, and subsequent mortality rate. The susceptibility and mortality rates are higher in Kids having low levels of serum immunoglobulin’s as compared to the Kids with adequate levels. The immunity/resistance to colibacillosis is transferred to the newborn animal immediately after birth from the dam through colostrum. The colostral immunoglobulin’s, which are responsible for such immunity, are generally absorbed for e to 24 hr after birth in Kids and u to 48 hr in goats.

The other factors, which influence the consumption of colostrum by the neonate are also significant in precipitating the disease. The important among them are the time of first intake of colostrum (absorption is more if consumed early); frequency of intake (more absorption with frequent intake); quantity of intake (immunity is better with adequate quantity, for Kids about 50 ml/kg b wt within first 8-12 hr); maternal behavior (dams may not allow sucking due to some reason); health and vigour of the newborn animal (weak animals are unable to suck adequate quantity); size, shape and number of functional teats (consumption of sufficient colostrum can be anticipated from normal udder and teats); number of parity (wide spectrum of specific antibodies would reasonably be present in the colostrum of mature cows); and the health of the dam. In addition, several management factors often play important role in causing the disease. The plane of nutrition and feeding practices are of greater importance. The susceptibility is increased if the dairy Kids are maintained on milk substitutes, if fed milk in containers rather than allowed to suck, and if fed irregularly.

Adequate hygienic and sanitary measures are also required to be adopted in the farm to minimize the incidence of colibacillosis in the newborn animals. Overcrowding of animals in a given area is one of the major predisposing factors for occurrence of the disease. It has also been observed that the incidence of colibacillosis increases if a particular farm is being used to maintain animals for a pretty long time without any depopulation or allowing a vacancy for cleaning out. Also, if lambing is allowed in sheds to avoid cold exposure during winter months, the sheds may soon become the source of infection leading to outbreak of the disease.
Pathogenesis

The diarrhoea can occur as a result of defective absorption of fluids, increase in secretions, and increased or decreased or normal intestinal motility. As a result of Reo virus infection, tall columnar intestinal epithelial cells are lost and replaced by low cuboidal cells. Corona virus attacks the columnar epithelial cells of the entire villi resulting in marked villous atrophy whereas Chlamydia destroys the epithelial cells of the villi and crypts. As a result of these infections, malabsorption occur leading to diarrhoea.

Colibacillosis in farm animals can occur in enterotoxic (manifested primarily by diarrhoea) and septicaemic (characterized by septicaemia and rapid death) forms caused by different serotypes of E. coli. Enterotoxic colibacillosis occurs more commonly in Kids and piglets as compared to lambs and foals. The enterotoxigenic strains of the bacteria on reaching the upper part of the small intestine of the susceptible new born, adhere to the intestinal epithelial cells mediated by bacterial pili. Bacterial fimbriae attach to specific receptor sites on villous epithelial cells. The organisms then colonise, proliferate to form micro colonies covering the villous surface, and produce enterotoxin, which induces increased secretion of fluid and electrolytes from the systemic circulation through the intact intestinal epithelium. It occurs as a result of enterotoxin stimulating the mucosal adenyl cyclase activity, which leads to increased cyclic AMP and thereby, increased secretion. The intestinal crypts as well as the villous epithelium are involved in such secretion and secreted fluid has alkaline pH, and as compared to serum it Is isotonic, has low protein and high sodium and bicarbonate values. The loss of such fluids, therefore, results into dehydrntion of varying degree, electrolyte imbalance, acidosis and hyperkalaemia.

If the disease is confined to intestine, the response to treatment is good in the early stages. But in severe cases, death may occur as n result of acidosis (which leads to circulatory failure and shock), electrolyte imbalance, and dehydration (due to hypovolemic shock). In Kids, particularly under one week of age, lactic acidosis may develop due to reduced ability to utilise lactic acid and severe hypoglycaemia may occur due to a reduced rate of conversion of lactic acid to glucose. It may be non- lactic acidosis in the Kids, which are more than I-week-old. In the piglets of I to 3 days age group, severe dehydration and metabolic acidosis may also occur. Simultaneous infection of rotavirus or other enteric pathogens may increase the severity of diarrhoea and other associated symptoms in Kids.

Septicaemic colibacillosis occurs more commonly in foals and lambs as compared to Kids and goats. It may affect Kids and piglets, which have received inadequate quantities of immunoglobulins. The invasive strains of E. coli, which invade the tissues and systemic circulation via intestinal lumen, umbilical vessels, tonsilar crypts or nasopharyngeal mucosae, are responsible for causing septicaemia. Intestinal permeability to macromolecules in goats may act as a predisposing factor for the entry of pathogen. The endotoxin produced by the organism is responsible for the septicaemia and subsequent shock in the affected newborn. The bacteria nay localize in different organs in the recovered animals causing either arthritis (commonly recorded in Kids. foals and lambs), meningitis (in Kids and goats) and polyserositis (in goats).
Clinical findings

Enteric colibacillosis occurs commonly during the first week after birth. The faeces become watery or pasty and usually chalky-white to yellow and often streaked with blood. Defecation is frequent, tail and buttocks are soiled and the faeces have an offensive rancid smell. There is usually a systemic reaction with rise in body temperature up to 105°F and an increase in pulse rate. The animal is unable to drink and becomes dull, listless and dehydrated. There may be abdominal pain on palpation, sometimes tenesmus is evident and the back may be arched. Without treatment, death usually occurs in 3_5 days following decreased heart rate, arrhythmia and terminal hyperkalaemia. In mild to moderate cases, spontaneous recovery may be recorded. All cases of colibacillosis should be carefully examine for evidence of omphalophebitis.

The severity of enterotoxic colibacillosis in Kids depends upon the type and number of the causative organism. A state of collapse referred as enteric-toxaemia may be caused by a single strain of E. coli. The major clinical signs in such cases arc cold clammy skin, severe weakness, wetness around mouth, collapse of superficial veins, coma, bradycardia, arrhythmia mild convulsive movements and periodic apnoea. Though diarrhoea may not be presents abdominal distension may be apparent. Percussion and auscultation of abdomen at this stage may reveal fluid splashing sounds suggesting presence of enough fluid in the intestines.

Septicaemic colibacillosis is an acute disease in the Kids during its first few days of life having no diagnostic clinical sign. Depression anorexia and marked tachycardia are the only abnormalities noticed. In this form, diarrhoea is not a consistent clinical sign. Body temperature, which may be high initially, subsides to become subnormal when diarrhoea and dysentery ensues and at this time the animal becomes weak and moribund. The post-septicaemic localization is usually seen about one week later in the surviving animals. The common signs are arthritis with lameness, pain and swelling in the joints, meningitis manifested by recumbency, opisthotonus, colic, paddling convulsions, nystagmus, and panophthalmitis with pus in the anterior chamber of the eyes. Pneumonia may also develop as a sign of localization, but is a less common sign.

The enterotoxic colibacillosis which is also known as 'baby goat diarrhoea' is commonly seen between few hours after birth to 3 days of age in goats, and is manifested by diarrhoea of varying degree (faeces may be pasty to watery, and colour may vary from yellow to brown), anorexia. Dehydration, straight and wet tail, weakness, lateral recumbency and paddling movements. The animal soon becomes more dehydrated and death usually occurs within 24 hr of onset of clinical signs due to electrolyte imbalance, acidosis, circulatory failure and shock. Generally, more than one goats or the entire litter of the sow is affected at a time and in severe cases, all the affected animals die within a very short period. The prognosis of the disease is favourable if correct treatment is provided at the onset of clinical signs.

Though less common in occurrence, septicaemic colibacillosis in piglets occurs during the first or second day following birth and usually the animals are found dead. Clinically, the affected piglets become weak, almost comatose, and cyanotic and have subnormal body temperature. In this infection, diarrhoea is often not a consistent finding and the prognosis is unfavourable as response to treatment is very poor.

In lambs, septicaemic colibacillosis is very common and occurs mostly in peracute form. The lambs of I to 2 days are susceptible. In peracute cases, the animals are found dead whereas the clinical signs in acute cases include collapse, stiff gait and other signs of meningitis. Later on the lambs become recumbent and hyperasthetic and show tetanic convulsions. Chronic cases are also seen in lambs where arthritis is a common finding.
Clinical pathology

Septicaemia or severe intestinal infection may be assessed by total and differential leukocyte counts while packed cell volume and the total solid concentration in blood could be helpful in assessing the degree of dehydration. The severe cases may reveal inadequate renal perfusion and thereby leading to kidney dysfunction. which may be reflected through high blood urea nitrogen values. There is reduction in bicarbonate, sodium and chloride ions whereas serum potassium is increased in severe acidosis.

The level of serum immunoglobulin in affected animals can help in assessing the prognosis of disease but such tests (usually zinc sulfate turbidity test) should be Inducted during first 24 hr after birth since the serum immunoglobulin levels tend to vary and become dependent on many other factors.
Necropsy findings


The autopsy should be performed immediately after death since autolysis of intestinal mucosa and invasion of tissues by intestinal microflora takes place very rapidly after death. Important changes in enteric colibacillosis in Kids include dehydration, distension of intestine with yellow watery content and gas, abomasal distension, and petechial haemorrhages in the abomasal mucosae. Microscopically, stunting and fusion of the villi of jejunum and ileum, infiltration of neutrophils and a layer of G -ve bacteria attached to the mucosa are seen. The gross lesions in piglets died of enterotoxigenic colibacillosis are more or less similar to those seen in Kids. In addition, villous atrophy and clotted milk in the stomach may also be found. In Kids where localization of the organism has taken place, omphalophlebitis, pneumonia, peritonitis and meningitis can be noticed.
Diagnosis


The diagnosis of enteric colibacillosis often becomes difficult because of the presence of other organisms in the intestine, which leads to inconclusive cultural isolation of the causative organism. The other commonly occurring diseases in newborn Kids where diarrhoea is seen are rotavirus infection, coronavirus infection, cryptosporidiosis, salmonellosis, coccidiosis and Clostridium perfringens type C infection. In piglets the similar diseases include salmonellosis, transmissible gastroenteritis, Cl. perfringens type C infection, rotavirus infection and coccidiosis. In lambs, Cl. perfringens type C and rotavirus infection may induce similar symptoms.

Rotavirus infection and Cl. perfringens type B are the diseases with similar clinical picture in the foals. Thus, for the definitive diagnosis or enteric colibacillosis the clinical, epidemiological, microbiological, and pathological findings are very much helpful. Tie enteric colibacillosis needs to be differentiated from dietary diarrhoea in which the faeces is voluminous, pasty to gelatinous, and the animal is bright and alert rather than depressed as in colibacillosis.

Septicaemic colibacillosis can be diagnosed on the basis of laboratory isolation of E. coll. Salmonellosis, listeriosis, pasteurellosis, streptococcosis, and pneumococcosis in Kids; streptococcosis and listeriosis in piglets; salmonellosis, listeriosis and erysipelosis in lambs; and actinobacillosis, salmonellosis, streptococcosis and listeriosis in foals may cause septicaemia and differentiation of colibacillosis from them is important to reach a conclusive diagnosis.

Isolation and identification of the causal agent by culture and determination of virulence are important in colibacillosis of farm animals. The commonly used specific laboratory tests to identify enterotoxigenic K 99+ E. coli include direct fluorescent antibody technique (FAT) and enzyme linked immunosorbent assay (ELISA) test. For culture, either faeces or intestinal contents can be used. A subsequent antibiogrm of the isolate may also be valuable at many occasions.

For definitive diagnosis of the disease, serological tests like FAT, ELISA and serum neutralization test (SNT) may be used. Reduced blood pH and bicarbonate values may be detected through blood gas analyzer, and haemato-biochemical studies reveal increased total plasma or serum proteins and blood urea nitrogen (BUN).
Treatment

The approach towards management of neonatal diarrhoea is aimed at change of the diet, correction of fluid and electrolyte imbalance, antimicrobial therapy and isolation of the sick animals. Though less well understood, restriction of feeding of milk may prove beneficial because of inability of the sick animal to digest milk. Instead, fluids containing readily absorbable energy (glucose) may be given. Milk may be introduced gradually after recovery. Dilution of milk by adding water is to be avoided SO that the normal clotting mechanism in the abomasum is not disturbed.

The change in fluid and electrolyte balance as reflected by dehydration, acidosis and electrolyte imbalances can be corrected either by parenteral administration or by oral supplementation. Parenteral administration of fluid and electrolytes is helpful managing severe and acute colibacillosis. In severe dehydration and acidosis, solutions containing bicarbonate ions are preferred over solutions containing lactates as the latter has to be converted to bicarbonate by the liver, which may not be functioning normally. The simple and the best way to use the parenteral fluid is to administer an equal mixture of isotonic saline (0.85%), isotonic dextrose (5%) and isotonic bicarbonate (1.3%) solution. The requirement of bicarbonate ions can be calculated by using the formula: body weight (kg) x base deficit (mmol/l) x 0.3 (a factor for extracellular fluid space).

The base deficit varies between 5 to 20 mmol/l with an arbitrary average of about 15 mmol/l. Accordingly a Kids weighing 25 kg would require 25x 1 5x0.3 = 112.5 mmol/l bicarbonate. Sodium bicarbonate 1 g, would yield 12 mmol of bicarbonate and thus, about 9.4 g of sodium bicarbonate or about 723 ml of isotonic (1.3%) sodium bicarbonate solution will be required. This amount may, however, be altered depending upon the exact clinico-pathological condition of the animal.

In severe dehydration where the animal has lost about 10-12% of body weight, hydration therapy should be given with 100 mi/kg b wt intravenously during first 1 to 2 hr a 50-80 mi/kg b wt/hr. It should be followed by maintenance therapy with 140 mi/kg b wt over next 8 to 10 hr a 20 ml/kg b wt/hr. The acidosis and dehydration should be corrected initially by using isotonic sodium bicarbonate solution and thereafter mixture of multiple electrolyte solutions should be given. In moderate dehydration, the initial dose of fluid may be made half. i.e. 50 mi/kg b wt in the first 1 to 2 hr and the rest of the regimen should be similar to that given in case of severe dehydration. If required, solutions containing potassium can be administered with extreme caution because of the danger arising out of its cardiotoxic property and already existing hyperkalaemia in such cases.

Oral fluids containing necessary electrolytes are beneficial only when given at early stage of the disease, and as a follow-up measure to parenteral rehydration therapy. The basic principle behind such therapy is that in enterotoxigenic colibacillosis, the intestinal wall remains intact so that absorption of glucose by active transport mechanism is continued and along with glucose, sodium and water are also absorbed. various ions/salt have advantages and disadvantages when given orally and accordingly several preparations have been used. A mixture suitable for oral use includes glucose-67.53°/o, sodium chloride- 14.34%, glycinle- 10.3%, citric acid- 0.81%, potassium citrate- 0.2 1%, and potassium hydrogen phosphate— 6.8%; 32 g of this mixture is dissolved in 1 liter of water to make an isotonic solution having a pH of 4.3. Another mixture contains glucose monohydrate— 152 g, sodium bicarbonate- 12.75 g, glycinle- 4.72 g, potassium chloride— 3.6 g, sodium chloride- 2.84 g, calcium phosphate- 1.33 g and magnesium sulfate— 0.76 g. It should be added to water to give 80 mmol/l of bicarbonate. These fluids are recommended for administration by stomach tube if the animals are unable to suck. Recovery following fluid therapy becomes apparent within a few hours, and continuation beyond 3 days usually does not yield much.

The use of antimicrobial in enterotoxigenic colibacillosis in neonatal farm animals is still under debate and many antibiotics and their combinations have been recommended. The commonly used drugs include chloramphenicol, neomycin sulphate, tetracyclines, sulphonamides, cotrimoxazoles, nitrofuraldezone and ampicillin. Parenteral administration of the antimicrobial drugs is preferred over oral administration because of the advantage that the enterohepatic circulation provides a concentration of drug in the intestinal lumen. These drugs, however, should not be continued for more than five consecutive days so that the drug sensitive intestinal flora are not expelled out and their replacement by pathogenic bacteria or fungi do not occur, similarly, treatment of colibacillosis with immunoglobulin's, intestinal protectants and parasympatholytic drugs has enough scope of controversy since variable results have been recorded on different occasions.