giardiasis

Preferred Scientific Name

• giardiasis

International Common Names

• English: cockatiel feather mutilation syndrome; cockatiel feather syndrome; feather picking; giardiasis in birds; giardiasis in ruminants; giardiosis
• French: lambliose
• Russian: lambliasis

Giardia
Giardia duodenalis
Giardia intestinalis

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.

blood and circulatory system diseases of large ruminants
blood and circulatory system diseases of small ruminants
digestive diseases of large ruminants
digestive diseases of pigs
digestive diseases of poultry
digestive diseases of small ruminants
skin and ocular diseases of poultry

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).

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).

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.

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).

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).

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).