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IdentityTop of page
Preferred Scientific Name
International Common Names
- English: cockatiel feather mutilation syndrome; cockatiel feather syndrome; feather picking; giardiasis in birds; giardiasis in ruminants; giardiosis
- French: lambliose
- Russian: lambliasis
OverviewTop of page
Antonie van Leeuwenhoek first described Giardia in 1681. Many names have been proposed for the genus such as Cercomonas (C.intestinalis) (Lambl, 1859); Giardia (Kunstler, 1882); Lamblia intestinalis (Blanchard, 1888); and Giardia lamblia (Kofoid and Christiansen, 1915), which was accepted for the human form. Filice (1952) proposed three species based on morphology of median bodies: G. duodenalis in mammals, birds, reptiles; G. muris in rodents; G. agilis in amphibians. Today there is still little agreement about the name, so G. intestinalis, G. duodenalis and G. lamblia are all used, although the latter two are now usually considered to be synonymous (Felice, 1952; Meyer, 1994; Farthing, 1999, Adam, 2001).
Giardia is found worldwide in humans and other animals primarily in the small intestine. As many as 40 species of Giardia have been identified based on the animal in which it was found: G. canis (dogs),G. cati (cats), G. bovis (cattle),G. caprae (sheep, goats), G. lamblia (humans). This idea of absolute host specificity is no longer considered correct (Meyer, 1994;Thompson et al., 2000).
Of Filice’s species, only G. duodenalis exhibits considerable genetic diversity. Since cysts of G. duodenalis cannot be distinguished morphologically, methods have been developed to characterize isolates, such as DNA amplification and sequencing, isoenzyme analysis, pulsed-field gel electrophoresis, restriction fragment length polymorphism analysis and polymerase chain reaction (Wolfe, 1992; Farthing, 1999; Adam, 2001). Using these techniques, researchers have identified new species of Giardia: G. microti in voles and muskrats (van Keulen et al., 1998), G. ardeae in herons(Erlandsen et al., 1990); G. psittaci in parakeets (Erlandsen and Bemrick, 1987). Two genetic assemblages worldwide, "Polish" (Groups 1 and 2, Assemblage A) and "Belgian" (Group 3, Assemblage B) have been identified which infect humans and other species of mammals (van Keulen et al., 1995; Ey et al., 1996, 1997; Monis et al., 1999; Thompson, et al., 2000). A ‘hoofed stock’ genotype has also been identified in pigs, sheep, goats, cattle and alpaca that is not found in humans (Ey et al., 1997). Hunt et al. (2000) has reported two different isolates in calves - Type I and Type II.
Giardia is important because it may/may not cause clinical illness, particularly in young animals, resulting in reduced weight gain which has economic impact for the producer. Problems are most often seen in high-density production, or in animals otherwise debilitated by disease or malnutrition. Different Giardia isolates may/may not have zoonotic potential.
Hosts/Species AffectedTop of page
Age, health status, hygiene of environment, nutrition all are risk factors for Giardia infection. Young become infected from environmental contamination or from animal to animal contact. Infected animals are more often seen when densely housed with a large number of animals, when animals of all ages are housed together, and when the quality and amount of colostrum fed is inadequate. A cool, damp environment allows longer survival of cysts that increases the risk of infection in animals. Nesvadba et al. (1982) reported no predilection for giardiasis in any cattle breed.
Giardia is primarily seen in pet birds such as cockatiels, budgerigars, lovebirds, parakeets, conures, parrots and macaws (Box, 1981; Scholtens et al., 1982; Fudge and McEntee, 1986; Filippich et al., 1998). Feather picking (‘cockatiel feather syndrome’) is a common sign. It is also seen in wild birds such as great blue heron (Georgi et al., 1986; Erlandsen et al., 1990), ibis (Forshaw et al., 1992; McRoberts et al., 1996; Upcroft et al., 1997), stork (Franssen et al., 2000), American bittern, little blue heron, western meadowlark, swamp sparrow (Travis, 1939), and poultry, waterfowl (Fudge and McEntee, 1986).
Young birds are more susceptible, can have high mortality and in chronic infections see recurrent diarrhoea and weight loss (Filippich et al., 1998). This may be the result of how birds are raised in very densely populated environments (Pesek, 2001). Prevention is based on good hygiene and management, keeping living quarters dry, reducing faecal-oral transmission by using wire-floored cages, and elevating food and water containers, (Filippich et al., 1998). Quarantine of new birds, avoiding overcrowding, and treatment of birds with clinical signs will decrease Giardia in a flock (Pesek, 2001).
Giardia is seen in weaned 1-2 month old pigs (Koudela, et al., 1991); in weanlings and nursing piglets (Xiao et al., 1994a); and in all ages of feral pigs (Atwill et al., 1997). Most infected animals are asymptomatic, although diarrhoea may occur (Koudela et al., 1991; Xiao, et al., 1994a). Risk of infection is higher when pigs housed on porous concrete floor than on slotted and wired floors, and infection can be delayed on well managed farms (Xiao et al., 1994a). Prevalences of 44% (Koudela et al., 1991) and 2.5% (Ajayi et al., 1988) have been reported in domestic pigs and 7.6% have been reported in feral pigs (Atwill et al., 1997).
Sheep and Goats
Giardia is primarily a problem in lambs and kids, usually with diarrhoea (Deas, 1959; Padmavathi, et al., 1978; Sutherland and Clarkson, 1983; Kiorpes, et al., 1987; Suteu et al., 1987a, 1987b;Taylor et al., 1993; Xiao et al., 1994b; Olson et al., 1995; Koudela and Vitovec, 1998; Majewska et al., 1998). In lambs, prevalence of infection from 19% to 68.6% has been reported (Taminelli and Eckert, 1989; Buret et al., 1990; Taylor et al., 1993) and in kids prevalence of infection from 10% to 50% have been reported (Taminelli and Eckert, 1989). Adult sheep have been reported to have Giardia with prevalences of 3.6 to 5.3% (Buret et al., 1990; Taylor et al., 1993), and adult goats have been reported with a prevalence of 18% (Suteu et al., 1987a). Xiao et al. (1994b) reported pre- and post-partum shedding of cysts in ewes. This periparturient cyst shedding increases the likelihood of lamb contamination while in maternity pens.
Giardia is primarily found in animals less than six months of age, but cattle of all ages can have Giardia in low numbers. Infection may/may not be associated with diarrhoea. (Deshpande and Shastri, 1981; Nesvadba et al., 1982; Buret et al., 1990; Xiao et al., 1993, 1994c; Rings and Rings 1996; Olson et al., 1997a, 1997b; O’Handley et al., 1999, 2000a; Wade et al., 2000a, 2000b). Prevalence of infection has been reported from 0.16 to 73% (Taminelli and Eckert, 1989; Diaz et al., 1996; Quilez, 1996; Olson et al., 1997a, 1997b; Bednarska et al., 1998; Majewska et al., 1998; Ruest et al., 1998; Vilchez and Pote, 1999; O’Handley et al., 1999, 2000a); Fayer et al., 2000; Wade et al., 2000b). Animals have been reported to be at higher risk of infection in the summer (Wade et al., 2000a) or in spring (Xiao et al., 1993), and when allowed to nurse the dam (Quigley et al., 1994).
In Greece, Giardia infection was reported in buffalo with 100% prevalence (Himonas et al., 1998).
DistributionTop of page
Giardia is found worldwide in mammals, including humans, and birds, reptiles, amphibians.
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
Infection with Giardia when asymptomatic shows no abnormality, but if symptomatic many changes are seen. Gross signs seen include villous atrophy, crypt hyperplasia and distortion, mucous and hemorrhagic diarrhoea, dark red, thickened mucosa in folds (Supperer, 1952; Botti, 1956, Kulda and Nohynkova, 1978; Kiorpes, et al., 1987; St Jean, 1987; Wolfe, 1992; Rings and Rings, 1996; Ruest et al., 1997; Koudela and Vitovec 1998; Farthing, 1999).
Histological signs seen include moderate to severe diffuse inflammation in the jejunal chorion; cellular infiltrate of the lamina propria with mononuclear cells especially plasmocytes; purulent cryptitis in the proximal jejunum; epithelial cell damage, blunting of the microvillous border of epithelial cells, and no eosinophilia (St Jean, 1987; Wolfe, 1992; Buret, 1994; Rings and Rings, 1996; Ruest et al., 1997; Koudela and Vitovec, 1998).
Birds show histologic changes classified as enterohepatitis, with a distended proventriculus, dehydration, hyperaemic intestines, and watery yellow to green droppings. An increase in serum SGOT has been reported (Panigraphy et al., 1978; Scholtens et al., 1982; Fudge and McEntee, 1986; Filippich et al., 1998; Bourke, 2001).
DiagnosisTop of page Clinical Diagnosis
Clinical diagnosis comes from the observation of certain key symptoms: abdominal pain, diarrhoea with blood or mucus, nausea, poor weight gain, unthrifty, soiling of fur or feathers, and dry wool in sheep (Turner and Murnana, 1932; Deas, 1959; Padmavathi et al., 1978; Scholtens et al., 1982; Kiorpes et al., 1987; Issac-Renton, 1991; Olson et al., 1995; Filippich et al., 1998; Bourke, 2001).
See Pathology section.
Acute giardiasis with diarrhoea must be distinguished from viral, bacterial, and other protozoan infections. Giardia has a longer incubation period than most other enteric pathogens. Chronic giardiasis must be distinguished from other protozoan and helminth infections, malabsorption, irritable bowel syndromes, and inflammatory bowel disease. It may mimic duodenal ulcer, hiatal hernia, gallbladder or pancreatic disease (Wolfe, 1992).
Microscopic examination of faeces for the detection of cysts by mucosal or wet faecal smears is inexpensive and quickly processed. The slides can be examined unstained, or by using a variety of stains such as Giemsa, Ziehl-Neelsen or iodine (Deas, 1959; Scholtens et al., 1982; Fudge and McEntee, 1986; Isaac-Renton, 1991; Wolfe, 1992; Rings and Rings, 1996; Koudela and Vitovec, 1998; Farthing, 1999). Flotation methods may be passive, or use a centrifugation concentration technique. Saturated sugar and salt solutions are too hypertonic causing distortion of Giardia cysts, so 1.18 spg zinc sulfate is the solution of choice (Kiorpes et al., 1987; Isaac-Renton, 1991; Rings and Rings, 1996). Since cysts are shed intermittently, examination of multiple fecal samples is recommended (Isaac-Renton, 1991; Wolfe, 1992).
Immunological tests have been developed for the detection of antibodies produced by the animal, or of antigens produced by the protozoa (Rosoff et al., 1989; Faubert, 1996; Garcia and Shimizu, 1997). Direct fluorescence antibody tests, and enzyme-linked immunosorbent assays (ELISA) are examples of two kinds of immunological tests commercially available (Mohan, 1993; Mank et al., 1997; Behr et al., 1997). An ELISA is more expensive then using a microscopy technique, but has been reported to be more sensitive (Behr et al., 1997; Mank et al., 1997). Antibodies in serum are found in infected and non-infected people, especially in endemic areas, so may not be useful for diagnosis (Wolfe, 1992; Farthing, 1999). Immunofluorescent staining of smears is used, but requires the use of a fluorescent microscope (Mohan, 1993; Xiao et al., 1994b, 1994c).
Biopsies, duodenal aspirates, endoscopy and radiographs of the small intestine are other available diagnostic tests (Kulda and Nohynkova, 1978; Wolfe, 1992; Farthing, 1999). Differences in the success of use of tests is related to technical expertise, care used in performing tests, and quality of reagents. No one method or combination of methods can detect all infections (Wolfe, 1992).
For field use or in developing countries, mucosal or wet faecal smears (wet mounts) with or without staining are inexpensive and quickly processed. Slides, cover slips and a microscope are the only equipment needed. All immunological testing is more expensive and requires specialized equipment.
Immunology of Disease
Both humoral and cellular immune responses are generated by the host to control the infection, to clear the organism, and to develop protective immunity. T-cell function is necessary for resistance development. Anti-Giardia antibodies, IgG, IgM, IgA, are detected during the course of infection. IgG persists for weeks or months. Antigenic variation (immunodominant cystein rich surface antigens) has been found on the surface of trophozoites whose purpose may be evasion of the host immune defense, and to enable organisms to survive in different intestinal environments (Wolfe, 1992; Faubert, 1996; Nash, 1997; Farthing, 1999; Adam, 2001).
List of Symptoms/SignsTop of page
|Digestive Signs / Abnormal colour of stool in birds, white, green, yellow faeces||Poultry:All Stages||Sign|
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Cattle & Buffaloes:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|Digestive Signs / Bloody stools, faeces, haematochezia||Cattle & Buffaloes:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|Digestive Signs / Diarrhoea||Cattle & Buffaloes:All Stages,Poultry:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|Digestive Signs / Flatulence||Cattle & Buffaloes:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|Digestive Signs / Mucous, mucoid stools, faeces||Cattle & Buffaloes:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|Digestive Signs / Parasites passed per rectum, in stools, faeces||Cattle & Buffaloes:All Stages,Poultry:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Diagnosis|
|Digestive Signs / Polyphagia, excessive appetite||Sign|
|Digestive Signs / Steatorrhea, fatty stools, faeces||Cattle & Buffaloes:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|Digestive Signs / Unusual or foul odor, stools, faeces||Cattle & Buffaloes:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|General Signs / Dehydration||Cattle & Buffaloes:Calf,Pigs:Piglet,Sheep & Goats:Lamb||Sign|
|General Signs / Generalized weakness, paresis, paralysis||Sign|
|General Signs / Increased mortality in flocks of birds||Poultry:All Stages||Sign|
|General Signs / Lack of growth or weight gain, retarded, stunted growth||Cattle & Buffaloes:Calf,Pigs:Piglet,Pigs:Weaner,Sheep & Goats:Lamb||Sign|
|General Signs / Polydipsia, excessive fluid consumption, excessive thirst||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Cattle & Buffaloes:All Stages,Poultry:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|General Signs / Weight loss||Cattle & Buffaloes:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sign|
|Pain / Discomfort Signs / Colic, abdominal pain||Cattle & Buffaloes:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|Skin / Integumentary Signs / Broken, damaged feathers||Poultry:All Stages||Sign|
|Skin / Integumentary Signs / Dryness of skin or hair||Cattle & Buffaloes:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|Skin / Integumentary Signs / Rough hair coat, dull, standing on end||Cattle & Buffaloes:All Stages,Sheep & Goats:All Stages||Sign|
|Skin / Integumentary Signs / Ruffled, ruffling of the feathers||Sign|
|Skin / Integumentary Signs / Skin erythema, inflammation, redness||Sign|
|Skin / Integumentary Signs / Soiling of the feathers, vent feathers||Poultry:All Stages||Sign|
|Skin / Integumentary Signs / Soiling of the vent in birds||Poultry:All Stages||Sign|
Disease CourseTop of page
Three clinical forms of infection are seen in animals: asymptomatic; acute disease; and chronic disease (Farthing, 1999). Clinical variation may relate to host factors (genetic or environmentally related), or to severity of infection in intestine. Animals with normal immune systems develop immunity with resolved signs (Sutherland and Clarkson, 1983; Hunt et al., 2000).
An asymptomatic animal is infected but has no clinical signs (Meyer, 1994; Rings and Rings 1996). Acute disease has signs of watery diarrhoea, with/without blood, which is short-lived (self-limiting within 2-4 weeks), mild fever, depression, dehydration (Isaac-Renton, 1991; Meyer 1994). Chronic disease has signs of diarrhoea with intestinal malabsorption, reduced appetite, weight loss, failure to thrive syndrome, little to no fever, semi-formed faeces, steatorrhoea, and anaemia. Immunodeficiency is associated with chronic giardiasis (Isaac-Renton, 1991; Meyer 1994; Rings and Rings, 1996; Farthing, 1999).
Diarrhoea is caused by luminal factors such as the trophozoites’effect on bile salts and fat absorption, inhibition of trypsin activity, possible disturbances in intestinal motility; and mucosal factors such as lectin activity that promotes adherence of parasite and contributes to brush border lesions, decreasing sodium mediated glucose transport (Rings and Rings, 1996).
EpidemiologyTop of page
Giardia is transmitted by the faecal-oral route via contaminated food and water, or by animal to animal contact. Risk factors for transmission include age, health status, temperature and moisture of environment, use of surface or untreated water, contaminated food, and break down in hygiene. High-risk animals are the young and immunocompromised. It is unknown how many cysts are needed to cause infection, but a susceptible host only needs a few cysts. The prevalence rates and number of cysts excreted varies from day to day. Wild and domestic animals may be reservoirs (Isaac-Renton, 1991; Farthing, 1999).
Giardia has a direct life cycle that takes 1-75 days, usually 7-9 days, to complete and has two life stages: trophozoite and cyst. If there is increased intestinal motility, trophozoites do not become cysts and are lost to the environment and quickly die. Cysts form in the lower small intestine, leave the host in faeces, and may/may not be immediately infective. Cysts are the environmentally resistant stage that is able to infect a new host (Meyer and Jarroll, 1980; Meyer, 1994; Rings and Rings, 1996; Farthing, 1999).
There are no intermediate hosts needed to complete the life cycle. Mechanical vectors may move cysts from one place to another via freshwater clams (Graczyk et al., 1997, 1999a, 1999b); flies (Doiz et al., 2000), birds (Graczyk et al., 1998), and fomites such as machinery, vehicles, equipment, feeding buckets, and clothing.
Impact: EconomicTop of page
Giardiasis has its greatest impact on the young who may have reduced weight gain that keeps them unmarketable longer. Even with no difference in feed intake, feed efficiency is impaired, and there is lower carcass weight in infected lambs (Olson et al., 1995).
Zoonoses and Food SafetyTop of page
Humans are reservoirs for other humans, and wild and domestic animals. Molecular epidemiology has demonstrated that forms of Giardia that infect humans also occur in other species of mammals, and that several host-adapted genotypes might represent distinct species. The greatest zoonotic risk is from genotypes in Assemblage A and to a lesser extent in Assemblage B. The ability to genotype may be a powerful predictive tool for providing direct evidence of the source of outbreak or of cysts (Majewska et al., 1998; Farthing, 1999; Thompson et al., 2000). This zoonotic potential means that veterinarians must be concerned about not only the health of animals, but of the humans who handle infected animals (Rings and Rings, 1996).
Giardia infections occur throughout the year suggesting that water is either contaminated often or the cysts are long lived. Cysts in water remain viable longer when kept at cold temperatures. When kept at 4°C or less, 40% of Giardia cysts are still viable after three months. No cysts survive longer than three weeks in water at 37°C. Manure spreading from agricultural operations may move cysts from the barn to fields. Pastured or free-roaming animals defecate wherever they may be and contribute to environmental contamination. Water may be contaminated by runoff from these fields, or by animals defecating in the water. An increased risk of infection has been reported with contamination of barns and pastures (Ruest et al., 1998).
Foodborne outbreaks in humans are not common but have been reported. Outbreaks of giardiasis have been associated with eating contaminated home prepared salmon, fruit salad, cold noodle salad, and in restaurants such foods as sandwiches, vegetables from a salad bar, and iced drinks (White, et al., 1989, Porter, et al., 1990, Quick et al., 1992, Mintz et al., 1993).
Waterborne outbreaks in humans may occur when water is untreated, inadequately treated, or when there is contamination of the distribution system, such as when there is mixing of water with raw sewage. Surface water is most often involved, although ground water may be contaminated. These protozoa may be found in water in the absence of E. coli, the normal indicator organism for faecal contamination (Craun, 1984; Rabbini and Islam, 1994).
Disease TreatmentTop of page
Giardia sp. infections in humans and other animals are treated with metronidazole, quinacrine, furazolidone and tinidazole (Upcroft and Upcroft, 1990; Rabbini and Islam, 1994). Sutherland and Clarkson (1984) reported treating kids with metronidazole (one oral dose of 600 mg/goat). Metronidazole and furazolidone are mutagenic, and quinacrine crosses the placenta so they are not approved for use in food animals in most developed countries (Edlind et al., 1990, Rings and Rings, 1996). Resistance of Giardia sp. to these drugs has been seen in recent years. This can be prevented by prudent administration, compliance of proper usage and avoiding their use as a prophylactic. (Upcroft et al., 1990; Upcroft and Upcroft, 1993; Townson et al., 1992).
Treatment of Giardia sp. infection has been successful using albendazole and fenbendazole that suppress cyst excretion by Giardia-infected calves (Reynoldson, 1994; Rings and Rings, 1996; Xiao et al., 1996). Xiao et al., (1996) reported using 20 mg/kg albendazole once daily/3 days orally and 1mg/kg-1 fenbendazole two times daily/3 days orally in calves. Fenbendazole (5mg/kg once daily/3 days) is an effective treatment in calves to eliminate Giardia, although multiple treatments may be required in infected animals. It is economical, has clinical benefit (fewer days with diarrhoea), and reduces the number of cysts being shed (O’Handley et al., 1997, 2000b). Benzimidazoles are inhibitors of polymerization of tubulin to microtubules that are components of flagella, the median body and the ventral disk of trophozoites. It is likely that the action inhibits attachment to the intestinal mucosa, not the movement by the flagella (Edlind et al., 1990; Jarroll, 1994; Adams, 2001). Flubendazol has been used to treat pigs for parasites including Giardia (Zizlavsky et al., 1998).
Alternative treatments use plant preparations. Methanolic extracts of 21 of 36 taxa of plants in Kenya and Tanzania were lethal or inhibited growth of Giardia (Johns et al., 1995), and isoflavones from Dalbergia frutescens stem bark in Venezuela hold promise, especially formononetin (Khan et al., 2000). Anti-giardial activity of a powdered preparation of Yucca schidigera (yucca) was tested in vitro and in vivo in gerbils and lambs. Lambs shed fewer cysts after several days of treatment, but a corresponding decline in prevalence was not seen (McAllister et al., 2001).
Filippich et al. (1998) treated birds with metronidazole in drinking water (800 mg/L of water for 5 days) and Panigraphy et al. (1978) used dimetridazole at a concentration of 0.02% water.
Histostat in feed and copper sulfate in water is used to treat histomoniasis, trichomoniasis and hexamitiasis in poultry (Penpages, 1999). Drugs with dosages are listed in Penpages (1999) and in Fudge and McEntee (1986). One holistic treatment for birds uses a combination of lactulose, Echinacea and apple cider vinegar in drinking water, but it is not a 100% cure. Before and after any treatment it is important to disinfect cages using10% bleach (Bourke, 2001).
Prevention and ControlTop of page
Prevention is attained when there is interruption of transmission, or prevention of ingestion of cysts. Young stock management that includes adequate colostrum and nutrition, lack of animal to animal contact, a clean and dry environment, separation of animals of different ages, cleaning and disinfection of housing equipment and feeding utensils, keeping feed free from faecal contamination, handling of healthy animals before sick animals, and using prophylactic measures such as vaccines is the best place to start. Since Giardia is found in many animals throughout the world and has the potential to be zoonotic there is a large uncontrollable reservoir in the environment. Treatment of water and disposal of manure so water is not contaminated are ways to control cysts in the environment (Rings and Rings, 1996; Farthing, 1999; Wolfe, 1992). A vaccine for dogs and cats to prevent clinical signs and reduce cyst shedding was recently developed (Olson et al., 2000), but no vaccines are available for other species at this time.
Cysts are killed by boiling, drying, freezing and heating. Heating manure to 65°C takes 24 hours to kill Giardia cysts, which suggests that composting manure properly may kill the cysts. Anaerobic digestion of sludge has been shown to inactivate cysts almost 100% (Gavaghan, et al., 1993; Van Praagh et al., 1993) and waste stabilization ponds in Kenya and France remove over 99% of the cysts (Grimason et al., 1993; 1996). Kay et al. (1998) reported that Giardia cysts were completely destroyed by alkaline hydrolysis. Most disinfectants, especially chlorine based ones, do not kill the cysts at the dilutions recommended by manufacturers for use around animals (Jarroll et al., 1984). Quaternary ammonium compounds and Alcide products rapidly inactivate cysts (Zimmer et al., 1988).
ReferencesTop of page
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