Ostriches have been farmed mainly in the Little Karoo region of the Republic of South Africa (RSA) for over a 100 years, initially linked to a highly fluctuating fashion feather market (Smit, 1963). Since the 1970s and 1980s there has been a rapid demand for ostrich leather products as well as fresh meat, leading to a corresponding increase in bird numbers with significant farming operations established first in other parts of the RSA as well as Southern Africa (Namibia, Zimbabwe, Botswana) and then in North America, Europe, the Middle East as well as China and Southeast Asia. It was estimated that the domestic ostrich population worldwide could number approximately 1.1 million birds (Deeming and Angel, 1996), but this number is certainly increasing rapidly. There is, however, a severe lack of scientific knowledge addressing the health aspects of this unique production animal (Smith et al., 1995; Jensen et al., 1992; Huchzermeyer, 1994).
Most health problems in ostriches occur during the first 3 months of life (Swart, 1988; Terzich and Vanhooser, 1993; Huchzermeyer, 1994; Allwright, 1996; Grilli et al., 1996) with mortality figures between 30–40% up to that age accepted by many as ‘normal’. Disease outbreaks can account for 80–100% mortalities in such young chicks, with ‘survivors’ remaining stunted. Although many of these are finally due to infectious causes, ostrich chicks are notorious for their susceptibility to various stressors, often manifesting as the so-called ‘ostrich fading chick syndrome’ (Figure 1). These stressors include nutritional deficiencies/imbalances, environmental fluctuations and social aspects. Furthermore, ostriches depend during the first 10–14 days of life or even longer on nutritional as well as passive immunological factors from yolk, suggesting an innate inability to fully utilise feed nutrients and to mount an effective immune response during this period.
Figure 1.Ostrich fading chick syndrome.
The adage ‘a healthy production animal is one that performs according to predictable production parameters’ is as true for ostriches as it is for cattle in feedlots, dairy cows, pigs or poultry. However, the extremely variable conditions experienced in different management systems and nutritional regimens as well as wide variations in genetics limit this consideration in ostrich production to ‘farm standards’ rather than ‘industry standards’ as in the more established types of animal production (Table 1). A holistic approach that accepts the production of ostriches as a continuous cycle where the quality at each stage is directly influenced by the previous stage has resulted in dramatic improvements in some production parameters. Two of the most commonly employed measurements, mortality before 3 months of age and growth during this period, will be used in the following discussion to illustrate the role of mannanoligosaccharides in achieving improvement.
Stimulation of non-specific immune response as demonstrated in a variety of species (Savage and Zakrzewska, 1996) by mannanoligosaccharides is another established mechanism that is probably playing a role in the improvements seen in immuno-compromised young ostrich chicks. A key factor in successful ostrich farming is the production of high quality ostrich chicks (Table 2) such that the critical first 3 months are begun without compromise.
Table 1. Some South African ostrich production parameters.
Table 2. Basic principles for the production of high quality ostrich chicks.
Gram-negative bacterial infections
E. coli is by far the most common species of Enterobacteriaceae isolated from clinically affected ostrich chicks. It causes both intestinal and extraintestinal infections in both man and animals and forms part of the normal gastrointestinal flora. E. coli causes mastitis and diarrhoea in cows and calves and septicaemia and enterotoxaemia in piglets, while poultry and ostriches present symptoms as sinusitis, airsacculitis, enteritis, hepatitis, pericarditis, septicaemia and yolk sac infections. The adhesion of E. coli to host tissue at the site of infection (mediated by appendages known as fimbriae or so-called adhesins) is an essential prelude to these numerous infections (Smyth et al., 1994).
Species- and tissue-specificity/tropism are often typical characteristics of certain E. coli serovars/strains. E. coli strains are classified according to the characteristics of their capsular (K), somatic (D), and flagellar (H) antigens, which determine to a large extent their respective pathogenicity. Fimbriae can be uncomplicated (Type 1) or be one of several other classes of complex morphological appearance. Type 1 fimbriae are found in at least 70–80% of all E. coli, including normal faecal isolates. It is believed that these fimbriae anchor E. coli to mucus in the intestine as well as to urinary tract mucus (Orskov et al., 1980). Type 1 fimbrial attachment is mediated through mannose-sensitive receptors. Adherence to urinary tract mucosa can indeed be blocked with anti-type 1 fimbrial monoclonal antibody or with a mannose-containing receptor analogue. Such interference inhibits the development of urinary tract infection (Abraham et al., 1985; Aronson et al., 1987).
It is likely that the same is true in the gastrointestinal tract, a more complex and difficult to study environment, as it was found that the number of chickens from which E. coli 15R (Type I fimbriae) could be recovered in controlled experiments were significantly lower (75 versus 15%) on a diet containing 4,000 ppm mannanoligosaccharide (Spring, 1996). Although adherence mediated by fimbriae determines the site of infections, virulence factors such as haemolysin, heat stable and heat labile enterotoxins, Shiga-like toxins and cytotoxic necrotising factor are responsible for the disease symptoms and the severity of the infection (Smyth et al., 1994).
The importance of bacterial infections to ostrich chicks is clear from Tables 3 and 4a and b with pathogenic E. coli the most commonly isolated primary pathogen. Several so-called ‘rough’ strains/opportunistics have been linked to endotoxaemic deaths in newborn compromised lambs (‘watery mouth syndrome’ ) so that the impact of E. coli infections in stressed ostrich chicks is likely to be much greater than that illustrated only by a list of the most common pathogenic types (Hodgson, 1993). The relative importance of the most common pathogenic serotypes isolated from ostriches by the Onderstepoort Veterinary Institute (OVI) Bacteriology Section is shown in Table 6d. Most of these could be clinically related to a primary enteritis syndrome.
Table 3. Number of investigations in the 1995/1996 and 1996/1997 seasons.*
Table 4a. Ostrich isolations by Bacteriology Section, OVI, for the periods 1 June 1995 to 31 May 1996 and 1 June 1996 to 31 May 1997.
Table 4b. Birds presented for bacteriological isolations.
There are no host-specific Salmonellae in ostriches as far as we know (Huchzermeyer, 1994), compared to the situation in chickens where S. pullorum and S. gallinarum play this role. Several non-pathogenic isolates of only academic significance are regularly isolated in several parts of the world (OVI records; Huchzermeyer, 1994; Vanhooser and Welsh, 1995; Welsh et al., 1997). In all investigations S. typhimurium was the most important pathogen, related to enteritis, multifocal hepatitis and splenitis with death as a result of generalised septicaemia. Screening tests (2,005 cloacal swabs, 2,573 serum samples) for S. gallinarum/pullorum, S. hadar and S. enteritidis on healthy 4–6 month old ostriches from Namibia are shown in Tables 5a and 5b. Investigations during the OVI Ostrich Unit’s diagnostic programme in 1995–96 and 1996–97 seasons are shown in Table 6e. Eight of these salmonella infections were typed as S. typhimurium.
Several Salmonella spp. (e.g. S. typhimurium 29E) display Type I fimbrial attachment mechanisms similar to those of E. coli, and have been used in controlled studies to demonstrate the effects of mannanoligosaccharide supplementation (Spring, 1996).
Table 5a. Salmonella isolations from healthy 4–6 month old ostriches from Namibia.
Table 5b. Serology results of salmonella screening assay.
This opportunistic agent is often present on contaminated surfaces and in natural water sources. It is often a sequel to severe stress, long-term antibiotic usage and concomitant with protozoal infections, e.g. Cryptosporidium, Balantidium. Infections are associated with any/all of the following: oral granulomas/ulcerations, conjunctivitis, severe enteritis, multifocal hepatitis and septicaemia (OVI records; Momotani et al., 1995; Huchzermeyer, 1994). See Table 6 for results from the OVI/Ostrich Unit diagnostic programme. The increase in cases (most of these very resistant to ‘standard’ antibiotics) parallel to the same tendency in yeast and fungal isolations is probably due to increased antibiotic use during the unusually wet season of 1996–1997.
Pseudomonas have similar adhesion mechanisms to E. coli and Salmonella spp. (Buxton and Fraser, 1977); but pathogenicity is related to extracellular products like pigments, proteases, haemolytic toxins and enterotoxins as well as the lethal exotoxin A (Quinn et al., 1994).
Table 6a. Specific bacterial pathogens isolated from ostrich chicks younger than 3 months: P. aeruginosa.*
Table 6b. Specific bacterial pathogens isolated from ostrich chicks younger than 3 months: C. perfringens.
Table 6c. Specific bacterial pathogens isolated from ostrich chicks younger than 3 months: yeast and fungi.*
Table 6d. Most common pathogenic E. coli types.*
Table 6e. Salmonella.*
Table 6f. Other isolates.
OTHER GRAM-NEGATIVE BACTERIA
Other Gram-negative pathogens include Klebsiella pneumoniae and Campylobacter jejuni. Klebsiella pneumoniae is an opportunist associated with airsacculitis and enteritis. Campylobacter jejuni is associated with severe chronic pseudomembranous typhlocolitis, sometimes in conjunction with viral enteritis and often becomes systemic (hepatitis) during stress periods. Affected birds are often poor growers; so-called ‘fading chicks’.
Clostridia are the most common Gram-positive pathogen in ostriches, with C. perfringens the most important (Table 6). C. colinum and C. diffıcile are also occasionally found (Huchzermeyer, 1994; Terzich and Vanhooser, 1993; Frasier et al., 1993). They are all associated with toxic, gas-forming inflammation of the gastrointestinal tract resulting in poor growth, recurrent diarrhoea and poor feed conversion rate. Many Clostridia have non-mannose sensitive receptor mechanisms, but are inhibited by the addition of Bio-Mos, a commercially-available source of mannan sugars derived from yeast cell wall material. It is speculated that the glucan portion of the yeast cell wall is the effective part in these instances.
Experimental evaluation of Bio-Mos in ostrich chicks
MORTALITY AND GROWTH PERFORMANCE
From the above it is clear that bacterial pathogens are a major cause of losses in ostrich production, and that most of them share the same adhesive mechanisms to the gastrointestinal mucosa. It was therefore hypothesised that the inclusion of Bio-Mos, a commercially available source of mannanoligosaccharide, would cause a general lower mortality rate, as well as a better growth performance. Bio-Mos added at 2 kg per tonne in the starter ration was evaluated on several farms during 1995–1996. Data from only one of these farms are shown in Figures 2 and 3 as several changes to management were made on the others that could confound the results. On the farm ‘Magalies Volstruise’ of Mr André Coetzee only Bio-Mos was added to an already above average management system. Mortalities were reduced on average by 5.5% compared to the mean over the 2 previous years.
Figure 2.Mortalities during the periods with and without Bio-Mos.
Figure 3.Growth curve comparisons for chicks hatched during February 1995 (control) and February 1996 (Bio-Mos) versus standard growth curve.
An expected growth curve has been established over time on this farm through weekly weighing of all chicks and is used as a standard management tool for evaluating performance for the first 10 weeks. This allows early detection of subtle, erosive conditions. Traditionally February is the worst month. This is at the end of the breeding season, and late summer rains cause wet conditions and sudden temperature fluctuations between 30°C (max.) and 12°C (min.) on this farm. Note that in the control comparison period (Figure 3) from week 6–10 the chicks grow more slowly and the deviation from the standard curve gets wider as time goes by. At 10 weeks of age chicks weigh on average only 8 kg, instead of 8 kg at 7 weeks of age.
Growth performance in 1996 when Bio-Mos was included follows the same trend as every year except that chicks stay on course longer, and that from week 8–10 chicks grow at the expected rate to reach approximately 10 kg at 10 weeks when in ‘normal’ months it is 10 kg at 8 weeks of age. Notice in Figure 2 the mortality during this period compared to the previous year (26–17.5%) which corresponds closely to the average of 7% lower mortality in 1996 over the whole year.
An estimate of the economic advantages of using Bio-Mos during ostrich chick rearing was derived using the 1997 production statistics and the following assumptions:
- Ostrich chicks consume 5.2 kg of starter feed until the age of 5 weeks. (Bio-Mos included at 0.2% = 11 g)
- Ostrich chicks consume 18.6 kg of starter/grower feed from 5 to 10 weeks. (Bio-Mos included at 0.1% = 19 g)
- Therefore 30 g of Bio-Mos were used in raising an ostrich chick to the age of 10 weeks.
Using the total amount of Bio-Mos sold to ostrich producers in 1997 and assuming 30 g Bio-Mos were consumed per bird, 166,667 birds received the product. Fifteen of the farms were contacted, all of which produce an average of 2–3,000 chicks per year (i.e. 40,000 chicks; 24% sample size). Estimated improvements varied from 5 to 20% fewer mortalities during the first 10 weeks. (In one case a 50–60% improvement was reported!) Thus, 5% more chicks (× 2,000 birds produced on average) equates to 100 extra chicks while 20% more chicks equals an added 400 chicks. With less than 5% mortality from 10 weeks till slaughter this could mean 95–380 extra slaughter birds.
Due to the importance of bacterial enteric pathogens as a major cause of mortality in young ostriches, the use of mannose oligosaccharides as an adhesionblocking agent has been very effective in lowering mortality in ostrich chicks less than 3 months old in South Africa. An average of 5–20% lower mortality, representing a tremendous financial benefit to the respective producers, was noted on 15 farms during 1997 representing 40,000 chicks from a total of approximately 167,000 ostrich chicks that were raised during this period on feed including Bio-Mos in South Africa.
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Authors: 1D.J. VERWOERD, 1A.J. OLIVIER, 2M.M. HENTON and 3M. VAN DERWALT
1 Ostrich Unit,
2 Bacteriology Section,
3 Salmonella subsection, Onderstepoort Veterinary Institute, Onderstepoort, Republic of South Africa