Status of Backyard Poultry in Nepal

Abstract

Poultry sub sector within livestock contributes 8% of AGDP. About 80% of country’s population lives in rural areas where backyard poultry (BYP) is widely prevalent which contributes 55% of total poultry population. The focus on BYP are due to its especial characters like ready source of meat, pest control, inexpensive to rear, income of poor families, dual purpose, no requirement of intensive knowledge, etc. BYP mainly constitutes indigenous breeds; Sakini, Ghanti Khuile, Puwankh Ulte, to a large extent by ducks, and a very little part occupied by turkeys. Cockerel Exchange Program has been carried out in many rural parts of country to upgrade the genetic character of local chickens. Few imported breeds like Ancona, Australop and Plymouth rock are also found. BYP relies on free range scavenging which is the sole cause of slow growth although they grew hardy. Marketing system in BYP is direct. Chicks are weaned from 5‐9 months and resumed egg laying between 11‐15 days after weaning. Hilly region has highest percentage of BYP followed by terai. Ethnically, Tharu community is at first to own BYP in terai region while Magars in hill. The average BYP size is 5-10 per house hold with maximum of 50. Age at first lay is 142 days with production of 160/hen/year having 2-3 laying cycles/year and brooding mortality as high as 40%. Disease status is not fairly documented except several HPAI outbreaks in 2010 across the country. New Castle disease and Roundworm infestation is most commonly encountered cause of mortality of BYP. Vaccination is mere practice unless government support programmes are in action. Currently new species like Giriraja, Koiler are under consideration and much work has been started to establish it.

Key Words: Backyard poultry, status, Nepal

Cystitis in Cattle

CYSTITIS IN CATTLE

Inflammation of the bladders, usually associated with bacterial infection, characterized clinically by frequent, painful urination (pollakiuria and dysuria) and the presence of blood (hematuria), inflammatory cells and bacteria in the urine.

ETIOLOGY

Occurs sporadically by introduction of infection into the bladder when trauma to the bladder has occurred or when there is stagnation of the urine. In farm animals the common associations are:

• Cystic calculus
• Ascending infection of bacterial population from genital or urethra
• Descending infection from nephritis
• Exciting factors like urolithiasis, prolong gestation, difficult parturition, stagnation, stricture of urethra etc.
• Contaminated catheterization
• Some corrosive chemicals or toxic substances may reach the bladder in large amount and may set up cystitis due to irrigation.
• As a sequel to paralysis of the bladder. A special case of bladder paralysis occurs in horses grazing sudax or Sudan grass and in horses with equine herpesvirus myoencephalopathy.

In the above cases, the bacterial population is usually mixed but predominantly E. coli. There is also the accompaniment of specific pyelonephritides in cattle and pigs, associated with C. renale and Eubacterium suis, respectively (Carl & Walton 1993). Many sporadic cases also occur in pigs, especially after farrowing. Common isolates from these are E. coli, Streptococcus, and Pseudomonas spp. Corynebacterium matruchotii causes encrusted cystitis in horses. Enzootic hematuria of cattle resembles but is not a cystitis.

PATHOGENESIS

Flushing action of voided urine removes the normally invading bacteria to the bladder before they reach the mucosa. Mucosal injury facilitates invasion but stagnation of urine is the most important predisposing cause. Bacteria usually enter the bladder by ascending the urethra but descending infection from embolic nephritis may also occur.

CLINICAL FINDINGS

• The urethritis that usually accompanies cystitis causes painful sensations and the desire to urinate.
• Urination occurs frequently and is accompanied by pain and sometimes grunting; the animal remains in the urination posture for some minutes after the flow has ceased, often manifesting additional expulsive efforts.
• The volume of urine passed on each occasion is usually small.
• In very acute cases there may be moderate abdominal pain, as evidenced by treading with the hindfeet, kicking at the belly and swishing with the tail, and a moderate febrile reaction.
• Acute retention may develop if the urethra becomes blocked with pus or blood, but this is unusual.
• Chronic cases show a similar syndrome but the signs are less marked. Frequent urination and small volume are the characteristic signs. The bladder wall may feel thickened on rectal examination and, in horses, a calculus may be present.
• In acute cases no palpable abnormality may be detected but pain may be evidenced.
• Endoscopic examination of the bladder of affected horses reveals widespread inflammation of the cystic mucosa and occasionally the presence of a cystic calculus.

 CLINICAL PATHOLOGY

• Blood and pus in the urine is typical of acute cases
• Urine may have a strong ammonia odour
• In less severe cases – urine may be only turbid. In chronic cases – no abnormality on gross inspection.
• Microscopic examination of urine sediment will reveal erythrocytes, leukocytes, and desquamated epithelial cells. Quantitative bacterial culture is necessary to confirm the diagnosis and to guide treatment selection.

NECROPSY FINDINGS

Acute cystitis is manifested by hyperemia, hemorrhage and edema of the mucosa (Herenda 1990). The urine is cloudy and contains mucus. In subacute and chronic cases the wall is grossly thickened and the mucosal surface is rough and coarsely granular. Highly vascular papillary projections may have eroded, causing the urine to be bloodstained or contain large clots of blood. In the cystitis associated with Sudan grass, soft masses of calcium carbonate may accumulate in the bladder and the vaginal wall may be inflamed and coated with the same material.

TREATMENT

• Antimicrobial agents are indicated to control the infection and determination of the antimicrobial susceptibility of the causative bacteria is essential. Based on the activity on pH antibiotics should be selected. Ampicillin, Trimethoprim and sulphadiazine, Nalidixic acid, Nitrofurantoin are effective.
• Relapses are common unless treatment is continued for a minimum of 7 and preferably 14 days. Repeated bacterial culture of urine at least once during and again within 7-10 days after completion of treatment should be used to assess the success of therapy. Recurrence of infection is usually due to failure to eliminate foci of infection in the accessory gland and in the bladder wall.
• The prognosis is poor because of difficulty of completely eradication of infectious cause and common secondary involvement of the kidney. Free access of water should be permitted at all times to insure a free flow of urine.
• Irrigation of bladder with 1:1000 Glycerine-acriflavin or Glycerine-proflavin.
• Use of acidifier to alter pH – bacteriostatic action (Ammonium chloride or Sodium acid phosphate)
• Dextrose saline for more urination and washing of the bladder

DIFFERENTIAL DIAGNOSIS

The clinical and laboratory findings of cystitis resemble those of pyelonephritis and cystic urolithiasis.

• Pyelonephritis is commonly accompanied by bladder involvement and differentiation depends on whether there are lesions in the kidney, determined by rectal examination but in many cases it is not possible to make a firm decision. However, the prognosis in pyelonephritis is less favourable than in cystitis. Thickening of the bladder wall, which may suggest a diagnosis of cystitis.
• Enzootic haematuria and in poisoning by the yellow-wood tree (Terminalia oblongata) in cattle and by sorghum in horses.  The presence of calculi in the bladder can usually be detected by rectal examination, by ultrasonographic examination, by endoscopic examination in female ruminants and in both sexes of horses, or by radiographic examination in smaller animals.
• Urethral obstruction may also cause frequent attempts at urination but the urine flow is greatly restricted, usually only drops are voided and the distended bladder can be felt on rectal examination used to assess the success of therapy. Recurrence of the infection is usually due to failure to eliminate foci of infection in the accessory glands and in the bladder wall.

REFERENCES

Carr, J. and Walton, J.R. (1993) Bacterial flora of the urinary tract of pigs associated with cystitis and pyelonephritis. Vet Rec 132:575-577.

Chakrabarti, A. (2011) Text Book of Clinical Veterinary Medicine. 3rd ed. Noida: Kalyani Publishers. Pp. 394-396.

Balagopalan, T.P. et al. (2009) Surgical Management of Urinary Bladder Fibroma in a Dog – A case report. In: Bhatia, N. et al. (eds.) Intas Polivet, 10 (1), pp.101-102.

Pamukcu, A.M. (1974) Tumors of the urinary bladder. Bull World Health Organ. 501(1-2): 43-52

Herenda, D. et al. (1990) An abattoir survey of urinary bladder lesions in cattle. Can Vet 31:515-518.

Radostits, O.M. et al. (2009) Veterinary Medicine- A textbook of the disease of cattle, horses, sheep, pigs and goats. 10th ed. Noida: Elsevier. Pp. 561.

Diarrhoea in Neonates of Farm Animals

DIARRHOEA IN NEONATES OF FARM ANIMALS

Category: Veterinary, Sub-category: Pathology,

Author/s: Krishna K Yadav, Level: B.V.Sc.& A.H.

Institute: Institute of Agriculture and Animal Science (IAAS)

Country: Nepal

Abstract: 

Some specific infectious agents have been associated with undifferentiated diarrhoea in neonates. Enterotoxigenic E. coli is probably the most common single cause of undifferentiated neonatal diarrhoea in calves during first week. Bovine coronavirus and Rotavirus are responsible for a significant proportion of neonatal calf diarrhoea, alone, together, or in combination with other agents. Disease due to these viruses may begin at any time in the first 1 or 2 weeks of life. Both produce villus atrophy by causing lysis or exfoliation of surface enterocytes. Cryptosporidium, a minute apicomplexan protist, is commonly associated with undifferentiated diarrhoea and villus atrophy in calves. It is most common in animals about 4-20 days of age. Cryptosporidia are recognized in the brush border of epithelium on villi, and in mucosal smears and faecal smears or flotations. Giardia, a flagellate protist, has been implicated as an etiologic agent in diarrhoea of calves and other young ruminants, but giardiasis is infrequently diagnosed in this context. Strongyloides infection may also cause villus atrophy and diarrhoea in calves as young as 2-3 weeks of age. Clostridium perfringens types B and C are usually associated with acute hemorrhagic enteritis and dysentery; infection with these organisms is rare. Salmonellosis occurs in calves as young as 4 or 5 days of age. It is especially common in stressed calves weaned to milk replacer and moving through sales barns as vealers. Coccidiosis due to Eimeria spp. in lambs and in kids may occur in animals as young as 3 weeks of age. In piglets less than 3 weeks of age are enterotoxigenic E. coil, coronavirus (transmissible gastroenteritis), Rotavirus, and Isospora suis.

Key Words: Undifferentiated diarrhoea, Neonates, Farm animals.

 Introduction: 

Most of the time neonates’ diarrhoea remains undifferentiated. In most of the cases of neonates diarrhoea, it is assumed to be due to colostrum feeding and sometimes correlated with the protozoans, but there are some specific agents that are associated with the cause of the neonates diarrhoea. In some cases the diarrhoea can be the result of nutritional problem like overfeeding of colostrum, weaning stress, abnormal change in ambient habitat and others factors. The diarrhoea associated with nutrition problem may be compensated without a great loss but the diarrhoea associated with infectious agents leads to the deteriorating condition of neonates and will directly hamper the overall performance of the animal in early as well as later stage of their life. Most common cause of undifferentiated diarrhoea in neonates is Enterotoxigenic E. coli, Coronavirus, Rotavirus, Coccidiosis, Strongyloides infection, and Giardia. These infectious agents seem to cause diarrhoea at specific age in specific species of animal neonates.

Diarrhoea in calves

About 10 infectious agents have been associated with undifferentiated diarrhoea in calves under about 3 weeks of age. Frequently, combinations of several of these agents occur together, or in sequence. The consequences of combined infections appear to be more severe than infections with individual agents. The diagnosis of these infectious problems in a herd can be complex, and examination of more than one animal early in the course of disease is desirable. Non-infectious diarrhoea and emaciation, resulting from the use of nutritionally inadequate milk replacers containing heat-denatured protein, must also be considered and eliminated when examining artificially reared animals. Enterotoxigenic E. coli is probably the most common single cause of undifferentiated neonatal diarrhoea in calves. The disease usually occurs within the first week of life, and is confirmed by specific immunofluorescent techniques in smears and frozen sections, or by culture and characterization of the organism as enterotoxin producing. Occasional cases of enterohemorrhagic colibacillosis, caused by Shiga toxin-producing E. coli and producing fibrinohemorrhagic enterocolitis, occur in calves, usually in the second week of life.

Bovine coronavirus and Rotavirus are responsible for a significant proportion of neonatal calf diarrhoea, alone, together, or in combination with other agents. Disease due to these viruses may begin at any time in the first 1 or 2 weeks of life. Both produce villus atrophy by causing lysis or exfoliation of surface enterocytes. Cryptosporidium, a minute apicomplexan protist, is commonly associated with undifferentiated diarrhoea and villus atrophy in calves. It is most common in animals about 4-20 days of age. Cryptosporidia are recognized in the brush border of epithelium on villi, and in mucosal smears and fecal smears or flotations. Giardia, a flagellate protist, has been implicated as an etiologic agent in diarrhoea of calves and other young ruminants, but giardiasis is infrequently diagnosed in this context.

Bovine Torovirus (Breda virus 2) disease seems rare. The pathogenesis and lesions caused by the Breda agent are similar to other coronavirus infections, though some crypt cell necrosis is reported in the small intestine.

Other virus includes Astrovirus infections which is usually subclinical, and their implication as a cause of diarrhoea in calves is rare. Several Noroviruses (family Caliciviridae, genus Norovirus; formerly “Norwalk-like viruses”), or bovine enteric Caliciviruses (BEC), have been identified from the feces of diarrheic calves, including Norovirus Jena, Newbury agents 1 and 2, and the Nebraska BEC. Enteroviruses are commonly isolated from the feces of clinically normal animals, and they are likely not associated with significant disease, though diarrhoea has occurred in some experimental studies. Birnavirus has also been isolated from the feces of diarrheic calves, but with no proof of pathogenicity.

A bovine enteric syncytial virus, a group B rotavirus, was a cause of diarrhoea in calves in a beef herd. Bovine parvovirus infects cells in crypts of Lieberkuhn in the small and large bowel, and may cause mild to moderate diarrhoea, particularly in the post weaning period. Bovine viral diarrhoea virus can be implicated in enteritis of calves as young as a week or so of age, on the basis of microscopic lesions in the small intestine and colon similar to those found in older animals, and by virus isolation, or antigen or genome identification. Chlamydophila infection is very rarely recognized in association with enteritis. It may be acutely necrotizing and exudative microscopically.

Strongyloides infection may also cause villus atrophy and diarrhoea in calves as young as 2-3 weeks of age. Enterotoxigenic Bacillus fragilis has been suggested as a cause of diarrhoea in neonatal calves, but its role is unproven. A number of other syndromes are usually distinguishable on the basis of gross lesions at necropsy in diarrheic calves.

Clostridium perfringens types B and C are usually associated with acute hemorrhagic enteritis and dysentery; infection with these organisms is rare. Salmonellosis, usually due to Salmonella typhimurium, or perhaps S. Dublin or S. muenster in enzootic areas, occurs in calves as young as 4 or 5 days of age. It is especially common in stressed calves weaned to milk replacer and moving through sales barns as vealers. Salmonellosis may mimic undifferentiated neonatal diarrhoea, perhaps in association with rotavirus, coronavirus, or Cryptosporidium. Or it may cause acute fibrinous enterocolitis, with septicemia in a proportion of cases.

Bovine herpesvirus 1 (Infectious Bovine Rhinotracheitis Virus) in calves under 2 weeks of age may produce gastrointestinal lesions associated with generalized infection; more commonly the enteric lesions occur alone or dominate the picture. Characteristic foci of necrosis in the mucosa of the fore stomachs, perhaps associated with focal ulceration of the abomasum and crypts of Lieberkuhn, are the typical findings. Mycotic rumenitis and abomasitis are complications secondary to infectious bovine rhinotracheitis in calves, or possibly following abomasal venous infarction in salmonellosis.

Diarrhoea in other neonatal ruminants (kids and lambs)

Undifferentiated diarrhoea in neonatal lambs is mainly associated with enterotoxigenic E. coli, rotavirus and Cryptosporidium; Giardia may contribute, but its significance is poorly defined. Astrovirus has been found in lambs and experimentally produces diarrhoea. An adenovirus antigenically related to Ovine adenovims-2 is reported as a cause of enteritis in goat kids. Salmonellosis may occur rarely in young lambs. Septicemia is more commonly associated with certain serotypes of E. coli, which may be the cause of “watery mouth” in lambs. Bacteroides fragilis, producing enterotoxin, has been implicated as a cause of diarrhoea in neonatal lambs. Causes of undifferentiated diarrhoea in young goats are poorly defined, but the problem appears to be minor under usual conditions of husbandry. A similar spectrum of agents may be expected and sought. Lamb dysentery, due to Clostridium perfringens type B in lambs and kids under 8-10 days of age is usually recognized at necropsy as severe hemorrhagic enteritis, occasionally with necrotic ulcers. Coccidiosis due to Eimeria spp. in lambs and in kids may occur in animals as young as 3 weeks of age (Foreyt WJ. 1990). Raised white plaques or polypoid masses of infected epithelium are found in the terminal ileum, perhaps associated with hemorrhage. Strongyloides may also be associated with diarrhoea in ruminants only a few weeks old.

Diarrhoea in neonatal swine

The agents commonly implicated in undifferentiated diarrhoea in piglets less than 3 weeks of age are enterotoxigenic E. coil, coronavirus (transmissible gastroenteritis), Rotavirus, and Isospora suis. Approach to the diagnosis of gastrointestinal disease Enterotoxigenic colibacillosis typically occurs in piglets under a week of age, and causes no specific gross or microscopic lesions, other than organisms’ adherent to the brush border of enterocytes. Rotavirus and Transmissible gastroenteritis virus (TGEV, coronavirus) infections cause villus atrophy, in contrast to most types of E. coli. Isospora suis tends to occur in piglets over 5-6 days of age. It is associated with villus atrophy, and in a minority of cases, necrotic enteritis in the distal small intestine. Meronts or gamonts may be found in mucosal smears, and in epithelium on atrophic villi in section. A number of other agents are less commonly associated with undifferentiated neonatal diarrhoea in pigs. Porcine epidemic diarrhoea virus (coronavirus 777) infection is similar to TGEV infection. Non group A rotaviruses, antigenically distinct from group A Rotavirus, produce similar lesions experimentally; group B cause epithelial syncytia, in addition. Adenovirus infection, most commonly evident as intranuclear inclusion bodies in epithelium on the dome over Peyer’s patch in tissue sections, may be implicated as a cause of villus atrophy in occasional cases. Enteroviruses, astroviruses, and calicivirus have poorly defined significance as pathogens in piglets, though a calici-like virus causes villus atrophy in genotobiotic pigs. Cryptosporidium infects the large and small intestine in swine, where it seems to play a minor role as an enteric pathogen. Salmonella and Klebsiella, though rarely implicated as pathogens, can cause villus atrophy and diarrhoea in neonatal pigs, and some strains of E. coli with the same capacity are rarely encountered.

Bacteroides fragilis is also rarely associated with diarrhoea. None of these bacterial infections are common in piglets. Strongyloides  ransomi, transmitted in the milk, may infect young piglets, causing villus atrophy, malabsorption, protein loss, and diarrhoea. Hemorrhagic and necrotizing enteritis due to Clostridium perfringens  type C in piglets in the first week of life is readily recognized at necropsy. C. diflicile also causes diarrhoeal disease in piglets in this age group, with a distinct suite of gross and microscopic lesions.

Diarrhoea in foals

In the young foal, undifferentiated diarrhoea may be associated with Rotavirus, Cryptosporidium, and Strongyloides. Enterotoxigenic E. coli and coronaviruses are not proven pathogens in foals. Actinobacillus equuli may cause severe diarrhoea and hemorrhagic enteritis, with lesions of bacteremia evident in other organs at necropsy. Salmonellosis in foals may be seen as fatal diarrhea with few gross lesions, or as fibrinous enterocolitis and septicemia, similar to that seen in older horses. Escherichia coli and Klebsiella pneumoniae, with occasional gram-positive infections, are common causes of neonatal septicaemia, predisposed by failure of passive transfer of immunoglobulin. Fibrinonecrotic enterocolitis in foals under a week of age may be due to Clostridium peringens type B or C. Rhodococcus equi may cause chronic diarrhea and wasting in foals. Pyogranulomatous ulcerative lesions of the large bowel, and purulent mesenteric lymphadenitis, often associated with chronic purulent bronchopneumonia, are characteristically found in R. equi infection. Enterococcus (Streptococcus) durans, an Enteroadherent coccus, has been associated with diarrhea in foals. Moderate atrophy of villi covered with adherent gram-positive cocci is characteristic; the large bowel is not colonized. Strongyloides westeri is capable of causing diarrhea in young foals occasionally. Tyzzer’s disease, which is restricted to foals under about 6 weeks of age, may be associated with diarrhoea. However, the liver lesion dominates the pathologic picture.

Conclusion

Diarrhoea causing dehydration, metabolic acidosis, and electrolyte depletion is an important cause of morbidity and mortality in neonatal piglets, calves, lambs, and kids, and to a lesser extent in foals. Some classes of agents occur in most species of large animals, and mixed infections may occur; these include Escherichia coli, coronavirus, rotavirus, and Cryptosporidium. These, and some other less common agents, produce diarrhoea in neonatal animals, the etiology of which cannot be readily differentiated on clinical grounds or on the basis of gross examination at necropsy. Undifferentiated diarrhoea of neonatal animals requires etiologic diagnosis if appropriate advice is to be rendered on prevention and management of the problem. Many of the agents involved are transiently present, or produce villus atrophy that is obscured by autolysis, hindering diagnosis. To overcome these obstacles, one or more live untreated animals in the early phase of clinical disease, and representative of the herd problem, must be examined. They should be killed and examined immediately using a necropsy procedure modified so that specimens of small intestine are fixed within a few minutes of death, and so that appropriate samples of tissue and content are quickly collected for etiologic investigation. In each species, undifferentiated diarrhea of neonates may be caused by other agents, in addition to the common bacterial, viral, and protozoal causes cited above. Conditions distinguishable at necropsy from undifferentiated diarrhea, and caused by a further array of pathogens, are also found in most species.