cryptosporidiosis in livestock and poultry
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IdentityTop of page
Preferred Scientific Name
- cryptosporidiosis in livestock and poultry
International Common Names
- English: crypto; cryptosporidiosis in cattle; cryptosporidiosis in chickens; cryptosporidiosis in goats; cryptosporidiosis in pigs; cryptosporidiosis in sheep; cryptosporidiosis in turkeys; cryptosporidiosis of the gastrointestinal tract in birds; cryptosporidiosis, cryptosporidium parvum; Cryptosporidium andersoni-associated production loss in dairy cattle; Cryptosporidium infections in livestock and poultry; Cryptosporidium muris-associated production loss in dairy cattle; respiratory cryptosporidiosis in birds
OverviewTop of page
Cryptosporidiosis is caused by protozoan parasites of the genus Cryptosporidium (family Cryptosporidiidae, order Eucoccidiorida, subclass Coccidiasina, class Sporozoasida, subphylum Apicomplexa). Cryptosporidium are small intracellular parasites, which occur throughout the animal kingdom and have been reported in many species of mammals, birds, reptiles, amphibians and fish.
The type species of the genus Cryptosporidium described by Tyzzer 1907 is C.muris, from the gastric glands of laboratory mice. A more complete description of the life cycle was published (Tyzzer, 1910) and subsequently a second species, C. parvum, was also described from laboratory mice (Tyzzer, 1912). C. parvum differed from the type species, not only by infecting the small intestine rather than the stomach, but also because the oocysts were smaller.
Following the initial discovery of Cryptosporidium, over 50 years passed during which the parasite was commonly confused with other Apicomplexa parasites, especially members of the coccidian genus Sarcocystis. The reason for this was that many Sarcocystis spp. have oocysts with thin walls that often rupture, releasing free sporocysts, and because each sporocyst contains four sporozoites like Cryptosporidium oocysts, a variety of named and unnamed species were erroneously assigned to the genus. Subsequent ultra structural studies, however, supported earlier light microscopy studies and showed that Cryptosporidium species possessed a unique attachment organelle (Hampton and Rosario, 1966), which is the key feature that currently defines the genus and family (Levine, 1985).
More than 20 'species' of Cryptosporidium parasite have been described on the basis of the animal hosts from which they were isolated, however, the lack of host specificity with many species has brought into question the validity of many species classified in this way.
For a while, limited transmission studies were used as evidence for the mono-specific nature of the genus Cryptosporidium, resulting in the widespread use of the name C. parvum for Cryptosporidium parasites from all kinds of mammals, including humans. Other Cryptosporidium parasites, such as C. meleagridis in turkeys (Slavin 1955), C. wrairi in guineapigs (Vetterling et al., 1971), C. felis in cats (Iseki 1979), C. baileyi in birds (Current et al., 1986) and C. saurophilum in lizards (Koudela and Modry, 1998), were however, considered to be separate species based on demonstrated biological differences from the established species C parvum and C. muris.
In recent years, molecular characterizations of Cryptosporidium have helped to clarify the confusion in Cryptosporidium taxonomy and validate the existence of multiple species in each vertebrate class. As a consequence, the complete taxonomy of the genus has undergone major revision based on a number of parameters that included not only morphology but also developmental biology, host specificity, histopathology, and sequence-based differences, within the ribosomal RNA (rRNA) gene repeat unit between individual isolates within a previously ‘valid’ species. Species definition and identification of this genus is therefore constantly changing, with the addition of new species based primarily on molecular criteria. Currently there are 13 valid species namely: C. hominis found primarily in humans (previously known as C. parvum Type 1), C. parvum, found in humans and other mammals (previously known as C. parvum Type 2), C. andersoni in cattle, C. canis in dogs, C. muris in mice, C. felis in cats, C. wrairi in guineapigs, C. meleagridis in turkeys and humans, C. baileyi in chickens, C. galli in finches and chickens, C. saurophilum in lizards, C. serpentis in snakes and lizards, and C. molnari in fish (Xiao et al., 2004).
Cryptosporidium species infect the microvillus border of the gastrointestinal epithelium of a wide range of vertebrate hosts, including humans (see Table 1). Infected individuals show a wide spectrum of clinical presentations, but the pathogenicity of Cryptosporidium varies with the species of parasites involved and the type, age, and immune status of the host. In many animals, Cryptosporidium infections are not associated with clinical signs or are associated with only acute, self-limiting illness. In some animals, such as reptiles infected with Cryptosporidium serpentis or individuals who are immunosuppressed, the infection is frequently chronic and can eventually be lethal.
Table 1. Valid species of Cryptosporidium
Rodents, camel, man
Cattle, camel, sheep
Cattle, sheep, goat, man
Man, monkeys, sheep
Chicken, turkey, Cockatiels, quails, ostriches, ducks
Finches, chicken, capercaillies
Hosts/Species AffectedTop of page
Cryptosporidium species that infect mammals
Mammals represent the largest group of animals infected with Cryptosporidium spp. The taxonomy of Cryptosporidium in mammals has been the subject of dispute and for some time only two species (C. parvum as the intestinal species and C. muris as the gastric species) were recognized (Tzipori and Griffiths, 1998). There are now considered to be 6 valid species in mammals, reported previously, and described in more detail below.
Over 150 species of mammals have been identified as hosts of C.parvum or C. parvum-like parasites. Most descriptions, however, have been based solely on microscopy, with no careful morphometric measurements or genetic or other biological data. Recent molecular characterizations, however, have shown that there is extensive host adaptation in Cryptosporidium evolution, and many mammals or groups of mammals have host-adapted Cryptosporidium genotypes, which differ from each other in both DNA sequences and infectivity.
Currently, it is considered that C. parvum consists of nearly 20 genotypes that have been associated with mouse, pig, bear, deer, marsupial, monkey, muskrat, skunk, cattle, and ferret, some of which may represent different species (Xiao et al., 2002a). Some genotypes are clearly being delineated as distinct species and include C.hominis (human genotype or genotype 1), C. parvum (bovine genotype or genotype 2), and C.canis (the dog genotype). It has therefore been suggested that the name, C. parvum be used for the Cryptosporidium parasites previously known as bovine genotype and avoid the use of C. parvum broadly for Cryptosporidium in mammals.
C. parvum bovine genotype or genotype 2, is therefore known to infect mainly ruminants (cattle, sheep, goats, and deer) and humans (Morgan et al., 1998a, 1999a).
The type species of Cryptosporidium was first described in the gastric glands of laboratory mice, but not wild mice (Tyzzer, 1907). A more detailed description of each life cycle stage was later provided, and all stages were found to localize in the gastric glands of the stomach (Tyzzer, 1910). The pathology appeared to be slight and infection appears to be non-pathogenic in mice.
Based solely on morphology, C. muris or C. muris-like oocysts have been found in the faeces of cattle in the several countries (Anderson, 1987, 1988, 1990,1991; Bukhari and Smith, 1996; Kaneta and Nakai, 1998) and camels in Iran (Nouri 2002). Because species identification was not confirmed genetically or experimentally, many of these authors qualified their findings by calling the organism C. muris-like. Recent molecular characterizations of C. muris and C. muris-like parasites have indicated that all bovine isolates are C. andersoni (described below).
C. muris can infect a wide range of additional hosts, including hamsters, squirrels, Siberian chipmunks, wood mice (Apodemus sylvaticus), bank voles (Clethrionomys glareolus), maras (Dolichotis patagonum), rock hyrax, bactrian camels, mountain goats, humans, and cynomolgus monkeys (Chalmers et al., 1997; Dubey et al., 2002; Gatei et al., 2002, Morgan et al., 2000, Torres et al., 2000).
C. andersoni infects the gastric glands of the abomasum of older calves and adult cattle. Oocysts of C. andersoni are not infectious for mice, chickens or goats. There are conflicting cross-transmission data on species specificity of C.andersoni and C. muris-like isolates, such that molecular methods are usually employed in cross-transmission studies to confirm species identification. Genetically confirmed C. andersoni infection has so far been found only in cattle, bactrian camels, and sheep (Xiao et al., 1999a,b).
Cryptosporidium oocysts have been observed in the faeces of dogs worldwide. The oocysts are morphologically indistinguishable from those of C. parvum and can also infect humans and bovines but not mice (Fayer et al., 2001). Confirmed C. canis infections have been found in dogs, coyotes, foxes, and humans.
Cryptosporidium oocysts observed in the faeces of cats were reported to be C. felis on the basis of oocyst morphology, host specificity and pathogenicity (Iseki, 1979). Molecular characterizations support the concept of C. felis as a valid species. All Cryptosporidium isolates from cats characterized have so far shown significant sequence differences from other known Cryptosporidium spp. and genotypes, but similarity to each other, even though they were from different geographic regions (Morgan et al., 1998b, 1999b). Confirmed C. felis infections have been found in cats, humans, and cattle (Bornay-Llinares et al., 1999; Caccio et al., 1999; Morgan et al., 1998b; Pedraza-Diaz, 2001).
Cryptosporidium wrairi has been described fromthe guineapig (Cavia porcellus) (Vetterling et al., 1971). Infection was not associated with diarrhoea or overt signs of coccidiosis, but only with enteritis in small guineapigs weighing 200 to 300 g (Jervis et al., 1966; Vetterling et al., 1971). Initially, cross-transmission studies and oocyst morphological studies suggested that C. parvum and C. wrairi might actually be the same species (Tilley et al., 1991). More recently, molecular characterizations have identified significant differences between C. parvum and C. wrairi at multiple genetic loci (Chrisp and LeGendre, 1994; Morgan-Ryan et al., 2001; Spano et al., 1997). These combined data, along with the fact that naturally occurring C. wrairi infections have been found only in guineapigs, strongly indicate that this organism is a different species from C. parvum.
Recent research has revealed that mice harbour a genetically distinct form of Cryptosporidium, which is different from C. parvum (bovine genotype 2). Only rarely is C. parvum (bovine genotype) found naturally in mice since it is predominantly a parasite of ruminants and some humans (Morgan et al., 1998a; Morgan et al., 1999a). Therefore, it is likely that the species described by Tyzzer in 1912 was not C. parvum (bovine genotype) but was, in fact, the mouse genotype and it is suggested that this will be named as a new species in the foreseeable future (Xiao et al., 2004).
There are probably many other cryptic Cryptosporidium species in mammals, all of which were previously assumed to be C. parvum. Limited cross-transmission studies have shown biological differences among some of the genotypes (Enemark et al., 2002).
Cryptosporidium species of birds
Cryptosporidium is a primary pathogen in chickens, turkeys and quail, causing respiratory and/or intestinal disease, leading to morbidity and mortality. Although infections have been found in over 30 species of birds, only three avian Cryptosporidium species have been named (Lindsay and Blagburn, 1990; Sreter and Varga, 2000). The three species of Cryptosporidium (C meleagridis, C. baileyi, and C galli) can each infect a broad range of birds, but they differ in predilection sites. C. meleagridis and C. baileyi are found in turkeys and chickens infecting the small and large intestine and cloacal bursa, but they differ significantly in oocyst size. C. baileyi is also found in the respiratory tissues such as the conjunctiva, sinuses, and trachea and can be a significant cause of respiratory disease. C. galli infects only the proventriculus of chickens and finches.
Developmental stages of C. meleagridis are found on the villus epithelium in the small intestine of turkeys and chickens. It is also the third most common Cryptosporidium parasite in humans (Pedraza-Diaz et al., 2001). The oocysts are indistinguishable from those of C. parvum. The parasite can infect other avian hosts such as parrots (Morgan et al., 2001; Morgan et al., 2000b). Molecular analysis has demonstrated the genetic uniqueness of C. meleagridis (Morgan et al., 2000b; Xiao et al., 1999b), although several subtypes of C. meleagridis have been described based on multilocus analysis (Glaberman et al., 2002a).
A second species of avian Cryptosporidium, originally isolated from commercial broiler chickens, was named C. baileyi, based on its life cycle and morphological features (Current et al., 1986). C. baileyi is probably the most common avian Cryptosporidium sp. and can infect a wide range of birds. It has so far been found in chickens, turkeys, ducks, cockatiels, a brown quail, gulls and an ostrich (Lindsay et al., 1990; Morgan et al., 2001; Pavlasek, 1993).
A third species of avian Cryptosporidium was first found in the proventriculus of chickenson the basis of biological differences, including oocyst size and morphology (Pavlasek, 1999, 2001; Ryan et al., 2003). Confirmed hosts of C. galli include finches (Fringillidae), domestic chickens, capercaille (Tetrao urogallus), and pine grosbeaks (Pinicola enucleator) (Ryan et al., 2003). Morphologically similar oocysts have been observed in a variety of exotic and wild birds including members of the Phasianidae, Passeriformes, and Icteridae (Ryan et al., 2003). Future studies are required to determine the extent of the host range for C. galli (Xiao et al., 2004).
Based on limited biological and molecular studies, it appears that there are several other distinct avian Cryptosporidium species in ostriches and quail and other species of birds (Gajadhar, 1994; Lindsay et al., 1991). Infection with a Cryptosporidium species in bobwhite quails infects the entire small intestine causing severe morbidity and mortality (Guy et al., 1987; Hoerr et al., 1986; Ritter et al., 1986). Several other new Cryptosporidium spp. have been found in birds by molecular analysis, such as a duck genotype in a black duck and two goose genotypes in Canada geese, all of which are related to intestinal Cryptosporidium species (Morgan et al., 2001, Xiao et al., 2002a).
Cryptosporidium species of reptiles
Even though a high prevalence of Cryptosporidium infections has sometimes been found in captive reptiles, few studies have attempted to identify the species of parasite involved. For quite some time, one species, C. serpentis (Levine 1980),was the only species identified in snakes. More recently, however, C. saurophilum was described in lizards (Koudela and Modry, 1998). Of all the animals, reptiles, especially snakes, are the most severely affected due to the chronic nature of cryptosporidiosis in these animals.
Cryptosporidium was initially reported as causing a severe chronic gastroenteritis belonging to three genera and four species of snakes (Elaphe guttata, Elaphe subocularis, Crotalus horridus, and Sansinia madagascarensis) (Brownstein et al., 1977). This species was subsequently named C. serpentis (Levine, 1980), and its taxonomic status subsequently validated by morphological and other biological data (Tilley et al., 1990). All developmental forms of this specieswere identified by ultrastructure in the gastric mucosa. It causes postprandial regurgitation and firm, mid-body swelling. Unlike avian and mammalian cryptosporidiosis, infections appear to occur in mature snakes, with a protracted clinical course, and, once infected, most snakes remain infected (Brownstein et al., 1977). In a subsequent study, a number of snakes, representing eight genera and 11 species from 3 continents were found to be infected with Cryptosporidium isolates that were considered to fall into five separate groups (Upton et al., 1989), possibly representing other species. So far, most isolates from snakes characterized by molecular analysis appear to be related to other gastric Cryptosporidium spp. (C. muris, C andersoni, and C. galli) found in mammals and birds (Morgan et al., 1999c). C. serpentis has also been isolated from savanna monitors (Varanus exanthematicus) and the isolates shown be genetically related to C. serpentis based on sequence analysis (Xiao et al., 1999a).
C. saurophilum was named following an extensive study of the faeces or intestinal contents from 220 wild and captive lizards of 67 species (Koudela and Modry, 1998). Six species of lizards in five genera were found to be passing oocysts, and was designated the type host. The site of infection in Schneider's skink (Eumeces schneideri) was the intestine and cloaca. No pathological changes were found in the intestine and cloaca of adult lizards, but weight loss, abdominal swelling, and mortality occurred in some colonies of juvenile geckos (Eublepharis macularius) (Taylor et al., 1999). Molecular characterizations support the existence of C. saurophilum and recent evidence suggests that C. saurophilum can also infect snakes (Xiao et al., 2004).
More Cryptosporidium species are likely to be present in reptiles, based on the study in snakes referred to earlier (Upton et al., 1989). Some of the reported isolates may represent oocysts of C. muris, the Cryptosporidium mouse genotype, or other species from ingested and infected prey (pseudoparasites), and such findings are frequent in snakes showing no clinical signs of infection (Morgan, 1999a). Turtles and tortoises are also known to be infected with distinct gastric and intestinal forms of Cryptosporidium (Graczyk et al., 1997, 1998b), and geckoes are known to be infected with a distinct cloacal form (Upton and Barnard, 1987). Another new species, C. varanii was found in an Emerald monitor (Varanus prasinus) (Pavlasek et al., 1995), but it is unclear at this stage whether this speciesis actually C. saurophilum.
DistributionTop of page
Cryptosporidial infection is reported as widespread in countries where active surveillance and monitoring programmes have been instigated. In other countries, whilst the presence of infection has been reported, detailed prevalence and incidence data is lacking. Those countries where disease has not been reported may be due either to its absence, or a lack of information or reported investigations.
C. parvum is ubiquitous and widely distributed parasitic infection and its presence has been reported from many countries worldwide (see distribution table). It is only recently that the complete taxonomy of the genus has undergone major revision and, as such, many reports of cryptosporidiosis due to C. parvum in both animals and humans may also need revision in due course.
C. andersoni has been reported in USA, Canada, Brazil, UK, Czech Republic, Germany, France, Denmark, Japan, India and Iran (Anderson, 1987, 1988, 1991; Peng et al., 2003; Ralston et al., 2003; Pena et al., 1997; Bukhari and Smith, 1996; Pavlasek, 1995; Kvac and Vitovec, 2003; Enemark et al., 2002; Satoh et al., 2003; Kumar et al., 2004; Nouri and Khalaji, 2003).
Although reports suggest that C. baileyi is probably the most common avian Cryptosporidium found in chickens, turkeys, ducks and other birds (Lindsay and Blagburn, 1990), there have been no reported studies to determine incidence and prevalence in poultry in any country.
There is little or no information on the distribution or prevalence of C. galli. As well as reports of this species from chickens, it has also been reported from various species of wild birds (Ryan et al., 2003), consistent with the possibility of a widespread distribution.
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
PathologyTop of page
Endogenous stages infect enterocytes of the distal small intestine, caecum and colon. Histopathological changes occur mainly in the jejunum and ileum with parasitic stages are seen on the surface of epithelial cells lining the jejunum, ileum, caecum and, occasionally in severe infections, the colon and rectum (Fayer and Ungar, 1986). The meronts and gamonts develop in a parasitophorous envelope, apparently derived from the microvilli and so the cell disruption seen in other coccidia does not apparently occur. However, mucosal changes are obvious in the ileum where there is stunting, swelling and eventually fusion of the villi. This has a marked effect on the activity of some of the membrane-bound enzymes.
The presence of the endogenous stages of the parasite leads to destruction of the microvilli of peptic glands, which may account for the elevated concentrations of plasma pepsinogen detected in infected hosts. Some infected animals exhibit reduced weight gain compared with uninfected controls.
Endogenous stages of C. meleagridis are found on the villus epithelium without appearing to invade host tissues (Slavin, 1955). There is villous atrophy and crypt hyperplasia in the ileum of affected turkeys and humans.
C. baileyi is primarily a parasite of the epithelial lining of the bursa of Fabricius and cloaca of chickens, and the trachea and the conjunctiva are lesser sites of infection. Villous atrophy, shortening of microvilli and enterocyte detachment are the major pathological changes associated with intestinal cryptosporidiosis. In respiratory cryptosporidiosis, gross lesions consist of excess mucus in the trachea, nasal mucosal congestion, and atrophic Bursa of Fabricius. There may also be mottled lungs, cloudy air sacs, mottled livers and swollen spleens (Hoerr et al., 1978; Dhillon et al., 1981). Cryptosporidia are found in the nasopharynges, trachea, bronchi, and Bursa, but are not seen in the small intestine. With the respiratory form of cryptosporidiosis, there is epithelial cell deciliation and hyperplasia, mucosal thickening and discharge of mucocellular exudate into the airways in young broilers. Bronchopneumonia may be present in severely infected birds.
Gross lesions are not evident but on histology the glandular epithelium of the proventriculus is colonised with endogenous stages of the parasite. Areas of the epithelium may be hypertrophic and hyperplastic (Blagburn et al. 1990).
DiagnosisTop of page
Oocysts may be demonstrated using Ziehl–Nielsen stained faecal smears in which the sporozoites appear as bright red granules. Speciation of Cryptosporidium is difficult, if not impossible using conventional techniques. Research effort has concentrated on the elucidation of the molecular composition of Cryptosporidium. Electrophoretically distinct patterns of oocyst wall and sporozoite antigens have been constructed for C. parvum, C. muris and C. baileyi. (Nina et al., 1992). Monoclonal antibodies (mAbs) have been produced that are specific to some of these polypeptides. These mAbs have the ability to distinguish sporozoites of C. parvum (potentially the most pathogenic species to mammals) from other cryptosporidia. Monoclonal antibodies have become the basis for alternative detection methods, which involve the use of immunofluorescence (IF) or enzyme-linked immunosorbent assays (ELISA) (Peeters and Villacorta, 1995). Commercially available ELISA and IF kits, based upon genus-specific monoclonal antibodies to oocyst surface proteins have allowed the transfer of these techniques to diagnostic laboratories. Although mAbs to genus-specific oocyst surface proteins are available, there are no mAbs that can be used to discriminate between species of intact oocysts. The detection limits of ELISAs and IF tests are similar to those stated above for the examination of stained faecal smears and depend primarily upon the concentration methods employed to prepare the sample.
More recently, DNA-based techniques have been used for the molecular characterizations of Cryptosporidium species using polymerase chain reaction; restriction fragment length polymorphism PCR-RFLP and sequence analysis of the small subunit (SSU) rRNA, Heat shock protein (HSP70) and Cryptosporidium oocyst wall protein (COWP) genes (Morgan et al., 1995, 1997, 1998a, 1999c; Spano et al., 1997; Sulaiman et al., 2000; Xiao et al., 2000).
Infections of cattle can cause varying degrees of dullness, anorexia, fever and loss of condition. Rarely do they cause the acute dehydration, collapse and high mortality seen with enterotoxogenic Escherichia coli or rotavirus, which can occur at a similar time. Infected weaned and adult animals normally exhibit obvious, identifiable signs of disease, such as scouring, however, infected animals with no signs excrete oocysts that can be transmitted to other susceptible hosts. Vomiting and diarrhoea have been reported in young piglets with combined rotavirus and Cryptosporidium infections.
Infected cattle do not develop diarrhoea, but can excrete oocysts, which are morphologically similar to, but slightly smaller than, those of C. muris (Lindsay et al., 2000).
C. meleagridis is associated with diarrhoea and a low death rate in 10 to 14-day-old turkey poults (Slavin 1955).
The presence of developmental stages in the microvillus region of enterocytes of the ileum and large intestines are not usually associated with clinical signs. Similarly, heavy infection of the bursa of Fabricius and cloaca does not appear to result in clinical illness. The respiratory form can result in severe morbidity and, on occasions, mortality with up to 50% of a broiler flock showing clinical signs, and mortalities may reach 10% (Lindsay and Blagburn, 1990). Initially, severe disease is accompanied by sneezing and coughing, followed by head extension to facilitate breathing. Conjunctivitis in several species of birds has been reported. Severe signs of respiratory disease can last up to 4 weeks after infection.
List of Symptoms/SignsTop of page
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Sign|
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Sign|
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Sign|
|Digestive Signs / Bloody stools, faeces, haematochezia||Sign|
|Digestive Signs / Diarrhoea||Sign|
|Digestive Signs / Diarrhoea||Sign|
|Digestive Signs / Mucous, mucoid stools, faeces||Sign|
|Digestive Signs / Palpable dilated bowel internal paplation||Sign|
|Digestive Signs / Parasites passed per rectum, in stools, faeces||Cattle & Buffaloes:Calf,Poultry:Young poultry,Other:All Stages,Pigs:Piglet,Sheep & Goats:Lamb||Diagnosis|
|General Signs / Dehydration||Sign|
|General Signs / Dehydration||Sign|
|General Signs / Fever, pyrexia, hyperthermia||Sign|
|General Signs / Generalized weakness, paresis, paralysis||Sign|
|General Signs / Generalized weakness, paresis, paralysis||Sign|
|General Signs / Inability to stand, downer, prostration||Sign|
|General Signs / Increased mortality in flocks of birds||Sign|
|General Signs / Increased mortality in flocks of birds||Sign|
|General Signs / Lack of growth or weight gain, retarded, stunted growth||Sign|
|General Signs / Lack of growth or weight gain, retarded, stunted growth||Sign|
|General Signs / Lack of growth or weight gain, retarded, stunted growth||Sign|
|General Signs / Polydipsia, excessive fluid consumption, excessive thirst||Cattle & Buffaloes:Calf,Poultry:Young poultry,Other:All Stages,Pigs:Piglet,Sheep & Goats:Lamb||Sign|
|General Signs / Reluctant to move, refusal to move||Cattle & Buffaloes:Calf,Poultry:Young poultry,Other:All Stages,Pigs:Piglet,Sheep & Goats:Lamb||Sign|
|General Signs / Tenesmus, straining, dyschezia||Sign|
|General Signs / Trembling, shivering, fasciculations, chilling||Cattle & Buffaloes:Calf,Poultry:Young poultry,Other:All Stages,Pigs:Piglet,Sheep & Goats:Lamb||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Sign|
|General Signs / Weakness, paresis, paralysis of the legs, limbs in birds||Sign|
|General Signs / Weight loss||Sign|
|General Signs / Weight loss||Sign|
|General Signs / Weight loss||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sign|
|Ophthalmology Signs / Conjunctival, scleral, redness||Poultry:Young poultry||Sign|
|Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes||Sign|
|Ophthalmology Signs / Purulent discharge from eye||Sign|
|Respiratory Signs / Coughing, coughs||Sign|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Sign|
|Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea||Sign|
|Respiratory Signs / Mucoid nasal discharge, serous, watery||Sign|
|Respiratory Signs / Purulent nasal discharge||Sign|
|Respiratory Signs / Sneezing, sneeze||Sign|
|Skin / Integumentary Signs / Rough hair coat, dull, standing on end||Sign|
|Skin / Integumentary Signs / Ruffled, ruffling of the feathers||Sign|
|Skin / Integumentary Signs / Soiling of the feathers, vent feathers||Sign|
|Skin / Integumentary Signs / Soiling of the vent in birds||Sign|
Disease CourseTop of page
Cryptosporidiosis is common in young livestock, especially cattle and sheep, although pigs, goats, horses and deer can be infected. C. parvum is a cause of scour in young, unweaned livestock, although weaned and adult animals can also become infected. Infections are usually mild (though occasionally they can be severe, but transient), resulting in varying degrees of morbidity, but generally low mortality. As for other pathogens, the young, old and immunocompromized are most susceptible to disease. Affected animals usually recover within 2 weeks of showing signs of illness (Taylor, 1995).
Seasonal peaks of disease have been reported to coincide with birth peaks in spring and autumn (Angus, 1988). Infection is predominantly seen in young calves less than 3 weeks old (Fayer and Ungar, 1986). The first calves to be born often become infected without showing clinical signs. In these calves the parasite multiplies producing large numbers of oocysts in the faeces, which contaminate the environment for calves that follow. Infection spreads rapidly, and later-born calves can become so heavily infected that clinical disease results. Symptoms of profuse watery diarrhoea, abdominal pain and dehydration may be followed by recovery and immunity to further clinical episodes. Disease is often associated with the presence of other organisms, notably enterotoxogenic Escherichia coli, Salmonella spp., Clostridium perfringens, rotavirus and coronavirus (Current and Blagburn, 1990), all of which are may contribute to the neonatal diarrhoea complex (calf scours) although evidence indicates that C. parvum is a primary pathogen in its own right (Angus, 1988). Disease associated with C. parvum has also been reported in newborn sheep, goats and deer and in non-domestic ruminants including antelope and oryx (Gregory, 1990). Symptoms in all species included diarrhoea, dehydration and death in some instances. Pigs, goats and horses can also be infected. Most porcine cryptosporidial infections are asymptomatic with the majority of infections occurring in 6- to 12-week-old pigs (Lindsay and Blagburn, 1991).
Generally considered to be non-pathogenic, although some studies have suggested that the parasite may cause reduced weight gain and interfere with milk yield in dairy cows (Esteban and Anderson, 1995).
C. meleagridis has, until recently, only been described in turkeys. No studies have been reported to describe the disease course in naturally infected birds.
Experimental infections in broilers produce no clinical signs, but birds are susceptible up to 30 days of age. Both the prepatent and patent periods are influenced by the age at infection and the infective dose (Taylor, 1993). Under field conditions, infection is known to occur in chickens less than 11 weeks of age, but not in adult birds (Fayer and Ungar, 1986). There is limited epidemiological data from commercial egg-layer pullets compared with from broilers (Dhillon et al., 1981; Itakura, 1984).
Only limited studies in chickens have been made under experimental conditions. The prepatent period is 25 days, and patency last about 6 days (Pavlasek, 1999).
EpidemiologyTop of page
A variety of mammals act as hosts to C. parvum but little is known of the importance of their involvement in transmitting infection to, or maintaining infection in domestic livestock. In young calves infection appears to be age-related with seasonal peaks of disease reported to coincide with birth peaks in spring and autumn. The first calves to be born often become infected without showing clinical signs, but become sources of infection for calves that follow. Infection spreads rapidly, and later-born calves can become so heavily infected that clinical disease results. In many instances where Cryptosporidium is diagnosed in animals, it appears that infections usually originate from the same host species. The primary route of infection is mainly by the direct animal-to-animal faecal-oral route. Thus in calves for example, overcrowding, stress of early weaning, transport and marketing, together with poor hygiene will increase the risk of clinical infections (Taylor, 1995).
In lambs, chilling due to adverse weather conditions in the neonatal period, mixed infections or nutritional or mineral deficiencies could exacerbate or increase the likelihood of disease. Infection in these cases is likely to be transmitted through grooming, nuzzling, coprophagy, or by faecal soiling by direct contact with infected animals. Infection may also occur indirectly through consumption of contaminated foods or environmental sources, including pasture and water (Taylor, 1995).
The epidemiology of infection has not been studied, although it is likely to be similar to C. parvum in cattle. Many calves are likely to become infected without showing clinical signs but become sources of infection for calves that follow. The primary route of infection is by the direct animal-to-animal faecal-oral route. Thus in calves for example, overcrowding, stress of early weaning, transport and marketing, together with low levels of hygiene will increase the risk of heavy infections.
A survey conducted in the USA showed an overall prevalence of 1.4% of 95,874 random bovine faecal samples (Anderson, 1991). Samples collected from dairy herds in the USA tend to have about twice the prevalence of feedlot samples (Anderson, 1991). In Scotland, UK, Bukhari and Smith (1996) found 23% of 109 dairy cattle to be infected. In the Czech Republic, 4 of 96 (4%) cows were reported to be passing oocysts (Pavlasek, 1995). A study of 887 Holstein-Friesian breed heifers imported into the Czech Republic showed that 4.5% of the cattle entering the country from France and 7.9% of those imported from Germany were passing C. andersoni oocysts (Pavlasek, 1995).
Transmission appears to be mainly by the faecal oral route although in the respiratory form, infection may be spread by coughing and sneezing.
Details on the epidemiology are lacking, although, as with other species, transmission can be considered to be mainly by the faecal oral route.
Impact: EconomicTop of page
There is little information on the economic impact of cryptosporidiosis in domestic animals due to the paucity of information on species distribution, incidence and prevalence. Infection with Cryptosporidium in livestock has become increasingly important to agriculture because of its ability to infect a wide range of domestic and wild animals, and, more importantly, humans. Outbreaks of human gastroenteritis caused by this parasite are commonly blamed on run-off from farming operations, most notably dairy operations, and it is often assumed that young calves are the source of the parasites in waterborne outbreaks. The consequences and economic impact of large-scale water borne human outbreaks have therefore, also to be considered in any economic impact assessment As an example, the city of Milwaukee in the USA was affected by a Cryptosporidium outbreak in 1993, resulting from a drinking-water filter failure. The outbreak infected an estimated 403,000, and led to the death of 120 people at a total cost of US $96.2 million (Corso et al., 2003).
Zoonoses and Food SafetyTop of page
Cryptosporidiosis is a frequent cause of diarrhoeal disease in humans, and several groups of humans are particularly susceptible to cryptosporidiosis. Humans can acquire Cryptosporidium infections through several transmission routes (Griffiths, 1998).
In paediatric and elderly populations, especially in day-care centres and nursing homes, person-to-person transmission probably plays a major role in the spread of Cryptosporidium infections. In developing countries, Cryptosporidium infections occur mostly in children younger than 5 years, with peak occurrence of infections and diarrhoea in children younger than 2 years (Bhattacharya et al., 1997). In immunocompromized persons such as human immunodeficiency virus-positive (HIV) patients, the incidence and severity of cryptosporidiosis increases as the CD4+ lymphocyte cell count falls.Zoonoses
In rural areas, zoonotic infections via direct contact with farm animals have been reported many times, but the relative importance of direct zoonotic transmission of cryptosporidiosis is not entirely clear (Miron et al., 1991). In industrialized countries, epidemic cryptosporidiosis can occur in adults by the foodborne or waterborne routes. Young farm animals such as calves, lambs, goats and piglets are commonly infected with C. parvum (Fayer and Ungar, 1986; Lindsay and Blagburn, 1991). Many human infections with the protozoon are derived from livestock, particularly cattle, either from direct or indirect contamination.Transmission in food
The reservoirs and transmission routes of Cryptosporidium spp. suggest a risk for human infections through contaminated food. Foodborne cryptosporidiosis has been suggested in some instances, but rarely confirmed. The ubiquity of these protozoa, their obligate parasitic nature, the variable, but possibly long, pre-patent period, and the potential for subsequent person-to-person transmission make epidemiological investigation difficult. In foodborne investigations, moreover, the source of contamination is rendered more difficult to identify because of the lack of sensitive detection methods or an equivalent to the bacterial enrichment culture (Casemore, 1990). Epidemiological features, such as indirect zoonotic transmission and environmental contamination, enhance the likelihood that food could be a route of transmission. Casemore (1990) proposed that livestock infection and water contamination are the two major causes of food contamination.
Several outbreaks of cryptosporidiosis due to contaminated food or water have been reported and studies have sometimes identified water as a major route of Cryptosporidium transmission in areas where the disease is endemic (MacKenzie et al., 1994).
The potential risks from foodborne cryptosporidiosis come from ingestion of fresh, raw or uncooked foods. Foodborne transmission has been reported following the consumption of certain foods, such as raw sausage, offal, chicken salad and milk (Besser-Wiek et al., 1996; Casemore et al., 1986; Casemore 1990, 1991; Galbraith et al., 1987; Gelletlie et al., 1997; Kacprzak et al., 1990; Nichols and Thom, 1985; Thomson et al., 1987; Wyllie, 1984,). An outbreak of cryptosporidiosis has been reported among people drinking freshly pressed, unpasteurized, cider, possibly resulting from faecal contamination of fallen apples by animals (Millard et al., 1994; MMWR, 1997). Outbreaks of cryptosporidiosis associated with contaminated drinking water have been reported from a number of countries including large outbreaks in the USA and UK (Bouchier, 1998).Food hygiene
Avoidance of contamination of vegetables and fruits in the field, strict hygiene measures involving handling of food and the susceptibility of the organism to freezing and cooking offer effective means of control. Contaminated water is another source of infection and appears relatively common and can result in large-scale outbreaks of disease. Improvement in water catchments may reduce the potential health risks associated with the presence of oocysts in water supplies, but would probably not eliminate the problem. The safety of bottled water varies from supplier to supplier. Heating water to temperatures above 72.4oC inactivates C. parvum oocysts (Fayer, 1994). Where oocysts of Cryptosporidium are detected in domestic water supplies, boil notices may be issued with the recommendation to boil water before drinking (Bouchier, 1998). Concentration of oocysts from water is possible by filtration of large volumes of water using cartridge or membrane filtration, or smaller volumes using a calcium carbonate flocculation technique (Fricker 1995). In food, similar concentration techniques may be applied before detection (Laberge and Griffiths, 1996).
Disease TreatmentTop of page
There is no known treatment (although spiramycin may be of some value) and the infection is difficult to control, since the oocysts are highly resistant to most disinfectants except formol-saline and ammonia. Symptomatic treatment may be given in the form of antidiarrhoeals and fluid replacement therapy. Halofuginone is available for the prevention of cryptosporidiosis in calves at a dose rate of 1mg/10kg bodyweight.
There are no reported treatments for other species of Cryptosporidium in their respective hosts.
Prevention and ControlTop of page
Good hygiene and management are important in preventing disease from cryptosporidiosis. Feed and water containers should be high enough to prevent faecal contamination. Young animals should be given colostrum within the first 24 h of birth and overstocking and overcrowding should be avoided. Dairy calves should be either isolated in individual pens or kept in similar age groups and cleaned out daily. On calf rearing farms with recurrent problems with C. parvum, the prophylactic use of halofuginone can be considered by treating for 7 consecutive days commencing at 24-48 h after birth.
On poultry farms, litter should always be kept dry and special attention given to litter near water fonts or feeding troughs. Fonts that prevent water reaching the litter should always be used and they should be placed on drip trays or over the droppings pit. Feeding and watering utensils should be of such a type and height that droppings cannot contaminate them. Batch rearing of birds, depopulation and adequate disinfection procedures should help limit levels of infection.
ReferencesTop of page
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