Open access peer-reviewed chapter

Giardiasis: Livestock and Companion Animals

Written By

Joyce Siwila

Submitted: September 23rd, 2016 Reviewed: September 7th, 2017 Published: December 13th, 2017

DOI: 10.5772/intechopen.70874

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Abstract

Giardia spp. are flagellates that are found in the intestinal tract of humans and domestic and wildlife animals, including birds and amphibians, worldwide. The genus Giardia comprises several species which are morphologically similar. Giardia infections have been reported widely in livestock and companion animals with varying prevalence in different parts of the world. Giardiasis, the disease cause by Giardia, may result in numerous episodes of diarrhoea, especially in young animals, which in turn adversely affect production resulting in economic loses. The affected animals may also act as a source of zoonotic infections. Evidence of infection in both animals and humans of Giardia duodenalis especially of assemblage A and B has firmly established giardiasis as a zoonotic disease. The zoonotic assemblage A and B have been reported in livestock (cattle, sheep, goats, pigs) and companion animals (dogs, cats, horses). However, questions regarding the direct transmission of Giardia from domestic animals to humans still need to be explored. Appropriate prevention and control measures are cardinal in preventing both animal and human infections. This chapter discusses G. duodenalis infection and the disease including treatment options in livestock and companion animals.

Keywords

  • Giardia
  • Giardia duodenalis
  • giardiasis
  • livestock
  • companion animals
  • treatment

1. Introduction

For years, man has relied on livestock for food, drought power, hides and other production activities. In less developed countries, livestock production is mostly done using traditional methods due to limited resources and these small-scale production systems accounts for most agricultural output in these countries [1]. On the other hand, companion animals are equally kept throughout the world. Dogs and cats are particularly kept as pets with increasing numbers in nations that previously did not do so but kept dogs mostly for security. Now, dogs are widely used for different purposes, including companionship, life-saving actions, security as well as hunting and farming [2, 3]. Other than entertainment and sports, horses are also being kept for companionship. These livestock and companion animals are however hosts to many parasites, some of which have detrimental effects on the health and productivity of those affected. Protozoa such as Giardia duodenalisaffect a wide range of domestic and wild animals, with serious clinical consequences especially in young animals.

G. duodenalis(syn. Giardia lamblia, Giardia intestinalis), a flagellate protozoan parasite, and the aetiological agent of giardiasis, is one of the most prevalent and widespread intestinal parasite in humans and several vertebrate animal species worldwide [4]. The taxonomy of the genus is mainly based on morphology and genetic evidence. According to these criteria, six species have been recognised in the genus Giardiaand these include G. duodenalisin humans and other mammals, G. agilisin amphibians, G. murisand G. microtiin rodents, G. psittaciand G. ardeaein birds. In recent years, phylogenetic analysis and enzyme electrophoresis have revealed the existence of eight assemblages A–H within the species G. duodenalis[57]. Giardiafrom humans appears to fall exclusively into Assemblage A and B while C and D are dog specific assemblages. Assemblage E is isolated from hooved animals, a characteristic of isolates from sheep, goats, cattle and pigs [8]. Cats are hosts F or Assemblage F while rats are hosts for Assemblage G [9, 10]. Assemblage H has been reported in the grey seal [11].

G. duodenalisis a frequently encountered intestinal parasite of domestic animals, especially livestock, dogs and cats. Giardiainfections have been reported widely in livestock and companion animals with varying prevalence in different parts of the world, but high frequency was mostly in dairy calves [1216]. As a parasite, Giardiahas a broad host range, however, the adverse consequences of infection and its pathogenic potential are best recognised in humans [6]. It causes an estimated 2.8 × 108 human cases per annum [17]. In Asia, Africa and Latin America, about 200 million people have symptomatic giardiasis with some 500,000 new cases reported each year [18]. Its simple life cycle involving an environmentally resistant cyst (Figure 1) provides greater opportunities for the parasite to be transmitted directly from one infected individual to another, or indirectly through contamination of the environment or food [4].

Figure 1.

Giardiacyst: wet smear stained with iodine (source:https://www.cdc.gov/dpdx/giardiasis/index.html).

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2. Transmission and clinical disease

The cyst is the infective stage and represents the resting stage of the organism. Its rigid outer wall protects the parasite against changes in environmental temperature, dehydration and chlorination, all of which would destroy the trophozoite [6, 19, 20] . Transmission occurs by the faecal-oral route, either by direct contact with an infected host, or through contaminated food or water [21, 22]. Mechanical transmission of the parasite through insect vectors has also been reported [23]. Factors that facilitate infection include overcrowding, the high excretion of cysts by infected animals and the low infectious dose (between 10 and 25 cysts) [24, 25].

Giardiais not invasive and therefore lives and multiplies by asexual multiplication on the luminal surface of the small intestine of the vertebrate host [6]. Although the pathogenesis of Giardiais not completely understood, the pathophysiological process is initiated by infection with the parasite resulting in variable clinical signs such as abdominal pain, diarrhoea and weight loss [26]. A rise in numbers of intraepithelial lymphocytes increases epithelial permeability. Activation of T-lymphocytes has also been observed in Giardiainfections [27, 28]. Trophozoite toxins and T-cell activation initiate a diffuse shortening of brush border microvilli and decreased activity of the small intestinal brush border enzymes, particularly lipase, proteases and disaccharidases [2931]. The microvillus shortening leads to a decrease in overall absorptive area in the small intestine and an impaired uptake of water, electrolytes and nutrients resulting in malabsorptive diarrhoea [29, 32]. The steatorrhoea and mucous diarrhoea usually observed in giardiasis are attributed to reduced activity of lipase and increased production of mucin by goblet cells [33]. Severity of the disease is dependent on factors like developmental, nutritional and immunity of the host as well as virulence factors of the parasite [30, 34, 35]. Although gross intestinal lesions are rarely observed, microscopic lesions consisting of villous atrophy and cuboidal enterocytes may be reported [33].

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3. Giardiasis in livestock

3.1. Cattle

In cattle, Giardiais considered an important emerging parasite of dairy cattle and also as a cause of zoonotic disease with negative effect on public health [19]. Calves have been reported to be infected with G. duodenalisas early as 4 days of age, and the highest intensity of cyst excretion of 105–106 cysts per gram of faeces between the ages of 1 and 3 months has been documented [36, 37]. A periparturient rise in cyst excretion has also been demonstrated [37]. Transmission occurs among infected calves as well as chronically infected adults [12, 38, 39] and is particularly high among dairy calves [38, 39]. There are four main proposed cycles of transmission that are believed to maintain host-specific and zoonotic assemblages of Giardiain mammalian hosts: human cycle, livestock cycle, dog/cat cycle and wildlife cycle (Figure 2). The livestock cycle is thought to maintain Assemblage E within the livestock group [6, 40, 41]. The other cycles maintain the assemblages in the specific hosts. For example, assemblages A and B can be maintained by direct transmission between humans, assemblage C and D between dogs (e.g. puppies in a breeding kennel) and wildlife genotypes among various wildlife species. Some assemblages, however, infect other animal species and humans. The frequency of transmission is however not very clear and still under debate. Zoonotic species have been reported in wildlife, but their role as a potentials reservoir for human infection still requires further molecular epidemiological research [4].

Figure 2.

Transmission cycles ofGiardia duodenalis(frequency of transmission is unknown).

The resultant giardiasis from G. duodenalisinfection can result in diarrhoea that does not respond to treatment with antibiotic or anti-coccidia drugs [33, 36, 42]. Giardiahas been implicated as an aetiological agent alone and in combination with other enteric pathogens in calf diarrhoea [36, 38, 43, 44]. Infection may also result in numerous diarrhoea episodes which in turn adversely affects production and result in economic loses for farmers [45]. In younger calves, especially below 6 months of age, the excretion of watery faeces with a mucoid appearance may be the only indication of infection with the parasite. Chronic cases of giardiasis in calves may impact negatively on performance which may be reflected in reduced weight gain, impaired feed efficiency and decreased carcass weight. This was demonstrated in experimentally infected lambs [43].

Giardiahas been found in both beef and dairy cattle throughout the world with varying prevalence. Infection rates can be as high as 100% [3638, 4650]. The infection pattern of Giardiaappears similar between beef and dairy cattle [36, 37] with cysts appearing in the faeces at approximately 4 weeks of age [12, 36, 38] . Both dairy and beef calves may harbour more than one genotype of G. duodenalis, which can be of zoonotic significance [12, 51, 52]. Assemblages A, B and E have been detected in cattle; Assemblages A and B also infect humans [53, 54]. As calves infected with Giardiashed large numbers of cysts, there is concern that cattle could represent a reservoir of G. duodenaliswith the potential to cause disease in humans either through direct contact or by contamination of food and/or water supplies [36]. Because of the risk of contamination of water supplies by water borne parasites such as Giardia, it is normally recommended that animal facilities should be located away from streams, lakes, dams and rivers whenever possible, and waterways should be fenced-off in pasture lands in order to prevent possible run-off into these water sources [55].

3.2. Sheep

The prevalence of G. duodenalisinfection in sheep varies considerably and may be as high as 38% in adult sheep and 68% in lambs [5660]. In a study in central China [61], the prevalence of G. duodenaliswas 12.36% in pre-weaned lambs and 5.74% in post-weaned sheep [61]. Other studies have also reported great variability in Giardiaprevalence: in Canada, prevalence of giardiasis was higher in lambs (57%) than in adults (9%) [62]; in Brazil, lambs had a 32% infection rate while that for ewes was 2%; [63]; and in Mongolia, China, lambs had a significantly higher infection rate than ewes (8.6 versus 0.9%, respectively) [64]. All the findings from these studies suggest that the infection rates of Giardiatend to decline as the age of the animals increases. However, the opposite has also been reported. In some studies in Australia, a much higher prevalence of was detected in post-weaned lambs and sheep (44%) than in pre-weaned sheep (11.1%) [56, 65]. In a study in Maryland, USA, the prevalence of giardiasis was higher in post-parturient ewes (12%) than in lambs (4%) [59]. Host age and immune status of the host affect the severity of the disease [6] but other factors such as the number of specimens examined, the age structure of the herds, management procedures and the health status of the animals may account for the discrepancies or variations in the infection rates in the different populations [61].

Because of the unexpectedly high levels of infection in sheep, sheep have long been considered a reservoir of human infections [56, 61, 6668]. In most cases, infections are asymptomatic but infected animals are carriers shedding large numbers of cysts into the environment [58]. Even if most infections are asymptomatic, infections in lambs may result in a malabsorption syndrome, decreased feed efficiency and subsequently a decreased weight gain and sometimes death [19, 43, 69]. In the study by [69], excretion of malodorous and poorly formed faeces was observed. Furthermore, giardiasis may have a negative effect on time to slaughter of the sheep [19, 43] therefore, negatively affecting producers’ income.

Three assemblages of G. duodenalishave been recognised in sheep, livestock assemblage E, and the two zoonotic assemblages A and B [13, 56, 59]. The non-zoonotic assemblage E is the most frequently reported compared to the zoonotic ones [59, 66, 68, 69]. However, assemblage E appears to occur most frequently in cattle compared to other livestock; this was demonstrated by an extensive, longitudinal study of dairy herds in Australia over several months and another study in Canada [12, 56, 70].

3.3. Goats

In small ruminants, there are considerably more surveys from sheep populations than goat populations and therefore fewer publications on Giardiain goats. Furthermore, only a few molecular studies regarding Giardiahave been performed worldwide [13, 58, 7174] compared to other ruminant hosts (see [4]). In the reported studies, Giardiaprevalence was reported to range from <10 to >40% depending on the age, geographical location and diagnostic technique used [75]. Infections are normally significantly higher in pre-weaned goat kids compared to that in older goat kids [74]. Most infections are asymptomatic, however, foul-smelling diarrhoea which is lightly coloured, greasy and mixed with mucous; reduced weight gain are clinical signs that may be observed, mostly in young animals that are symptomatic [71]. A study in Spain reported a high infection rate in young animals, agreeing with the hypothesis that to a great extent, young animals contribute to the environmental contamination with Giardiacysts [71]. A study in Nigeria also reported a high prevalence (46.9%) in goats with pre-weaned (≤3 months) goats having a much higher prevalence (58.1%) compared to those that were over 3 months (38.2%) [74].

Even though a large number of G. duodenalisgenotyping studies in ruminants report a higher occurrence of genotype E, with genotypes A and B being less frequent [13, 58, 76, 77], other studies, [13, 72] have reported zoonotic genotype A infections in goats in Belgium and Côte d’Ivoire, respectively. In Malaysia, one study [73] reported genotypes A and B in goats. These findings suggest that goats could be a potential source of zoonotic infection.

3.4. Pigs

There is limited information on the Giardiainfections in pigs. From the limited studies, Giardiainfections have been reported in all age groups from nursing piglets to boars and sows worldwide, from Australia, Asia, Europe and North America, Africa with varying prevalence ranging between 0.1 and 20% [62, 7886]. Natural infections are typically asymptomatic with no evidence of illness.

Both assemblages E and A have been identified in pigs with assemblage E being most common [4]. In one study in Australia, assemblage E was the most common genotype detected in positive specimens of both pre-weaned (64%) and post-weaned (67%) pigs [87]. In Denmark, assemblage E was also the most common genotype, being identified in 62% of samples from post-weaned pigs, while assemblage A was detected in only 12% of specimens [85]. Interestingly, the canine assemblage D has also been reported in pigs [85, 88].

Since pigs also harbour the zoonotic assemblage A, they should be considered as potential sources of infection. One case–control study in eastern England found an association between giardiasis and exposure to farm animals, pigs included [89].

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4. Companion animals

4.1. Dogs and cats

Giardiais commonly recovered from the faeces of both symptomatic and asymptomatic dogs worldwide [90, 91]. Several studies have reported high prevalence of Giardiain stool samples of companion animals (i.e. cats and dogs) (reviewed by [92]). Giardiainfection rates in dogs differ considerably based on many variables, including the composition of dog populations (owned/stray/kennel), the test used for diagnosis and its sensitivity. Similar to other animal species, severity of disease depends on host age and ability of the immunity to eliminate the infection. Reports of giardiasis range from 0.1% in owned dogs to as high as 100% in kenneled dogs, the risk factor being overcrowding and intensive contact between large numbers of dogs sharing the same shelter in kenneled dogs. This favours transmission of infections [6, 15, 9396]. Some studies have indicated Giardiato be the most common enteric parasite of dogs and cats. For example, studies in Australia found that G. duodenaliswas the most common enteric parasite of domestic dogs and cats [97, 98] while [99] also reported the parasite to be widely prevalent in dogs and cats in the USA. The prevalence of Giardiain these companion animals is however, believed to be underestimated because of the following reasons: the low sensitivity of the conventional detection methods, cyst excretion is intermittent and the disease is usually subclinical [98].

In most of the studies that have been conducted in dogs, puppies, free-roaming dogs, and shelter dogs have been shown to be at higher risk for infection than adult dogs and owned dogs [15, 94]. Transmission of the parasite appears to be maintained within the dog/cat cycle (Figure 2) as evidenced from the host specific assemblage C/D and F commonly isolated in dogs and cats respectively [15, 100]. However, zoonotic transmission of Giardiabetween humans and dogs in the same household has been reported previously [101]. In another study in Brazil, zoonotic assemblage A1 was isolated from dogs and children in the same locality suggesting the existence of a zoonotic cycle of the parasite in that community [102], and a study in Thailand revealed that dogs were a potential source of Giardiainfections for humans [103]. In this study [103], assemblages A (79%) and B (21%) in addition to the dog specific assemblages C (12%) and D (31%) were isolated from the 104 dogs tested. In the United States, one study reported that 28 and 41% of client-owned dogs presenting with infection with Giardiato veterinary clinics had potentially zoonotic assemblages A and B, respectively, while 15 and 16% had host specific assemblages C and D, respectively [104]. The findings from the American study suggest the possibility of the potential for transmission of non-canine-specific assemblages from owners to their dogs as well as zoonotic transmission from dogs to humans. Furthermore, such reports highlight the possibility of two transmission cycles existing in domestic urban environments, that is, transmission of dog-specific assemblages among dogs and the possible transmission of assemblage A between pets and humans. However, it has been reported that in household dogs, the frequency of dog-to-dog transmission may be lower because they are less crowded than kenneled dogs where prevalence is normally higher due to intensive contact among a large number of dogs [54, 91].

Although Giardiais common in dogs and cats, it is rarely associated with clinical disease and affected animals suffer minimal consequences of the disease, but may act as a source of zoonotic infection [103, 104]. However, complications such as persistent infections and impairment of growth and development may occur especially in young animals such as puppies and kittens [105]. Such infections with manifestation of clinical signs are usually associated with kennel or cattery setup, where there is overcrowding [106].

4.2. Horses

There is very few data on Giardiain horses and giardiasis is an uncommon condition in these animals. However, the parasite may be commonly found in faeces of asymptomatic animals. The parasite was first reported in horses in South Africa in 1921 [107]. Since then a number of reports have been made regarding the presence of the parasite in horses of all age groups. Relatively high rates of giardiasis among foals (17–35%) and lactating mares (1.9–27.8%) have been documented using the fluorescent antibody method [38]. Lower rates have been observed in weanlings (0–9.1%) [108]. Varying prevalence of giardiasis has been reported in different geographic areas and they differ considerably between locations [62, 109, 110] with age and physiological status of the animal playing an important role in the infection rates [38, 110].

Although giardiasis in horses has been found to be associated with diarrhoea, poor hair coat, ill thrift and weight loss [111, 112], infected horses rarely show any clinical signs [108] and no subclinical consequences have been reported previously. However, infected horses may show signs ranging from a mild and self-limiting to, occasionally, severe diarrhoea (with heavy infections). These are commonly seen in young and aged or immunologically suppressed horses [110, 113, 114]. However, some studies have reported no shedding of Giardiacysts in young and older horses [115].

G. duodenalisassemblages A, B, and E have been detected in horses [110, 116]. A study in Italy also confirmed the presence of both animal and human sub-assemblage of G. duodenalisin horses [117]. However, assemblage E appears to be more common in these animals [110]. Because assemblages A and B are known to infect humans [6, 118], horses could represent a reservoir of G. duodenaliswith the potential to cause disease in humans through direct contact or by contamination of food and/or water supplies.

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5. Diagnosis

The diagnosis of giardiasis is commonly established by microscopic identification of cysts or less commonly trophozoites in faecal specimens stained with trichrome (Figure 3) or iron haematoxylin. This follows the application of faecal concentration techniques, especially zinc sulphate flotation and centrifugation [119]. Direct smear or wet mount examination for trophozoites can also be performed. However, because of the cyclical nature of cyst excretion, several samples need to be examined to detect the organism [120]. The disadvantage of microscopy is that it is of limited epidemiological value as it does not indicate the source of the infection [6].

Figure 3.

Giardiacysts stained with trichrome stain (source:https://www.cdc.gov/dpdx/giardiasis/index.html).

Faecal immunoassays have been developed and these have improved the sensitivity of detecting the parasite in faecal specimens. The sensitivity and specificity of different assays is reported to range from 87 to 100% [121, 122]. Enzyme-linked immunosorbent assay (ELISA) is the mostly used immunoassay and it has enhanced the detection of the parasite in field samples and a number of kits are commercially available [120]. Furthermore, the development of direct immunofluorescence microscopy (antigen detection) has generally improved the sensitivity of detecting and quantifying faecal Giardiacysts and may allow for more accurate determination of prevalence rates and cyst excretion intensities compared to the conventional microscopy [46]. However, despite antigen detection being more sensitive than conventional microscopy, the method cannot discriminate between species or morphologically similar organisms. The other disadvantage is the need for a fluorescent microscope which is costly [123].

To overcome the non-discriminatory nature of the conventional microscopy, molecular techniques, particularly PCR-based procedures have been developed and have greater sensitivity and specificity than the techniques that rely on microscopy and/or immunodiagnosis [98]. For example, in a survey of dogs in India, microscopy detected only 3% prevalence compared to 20% with PCR [101]. The molecular methods are also able to provide information on the genotypes and species of Giardia, information that is necessary for determining the source of infection. PCR, when combined with restriction fragment length polymorphism (RFLP) analysis is faster when compared to sequencing which is also costly [124]. Although PCR has high sensitivity, results may be affected by amplification inhibitors and barriers to DNA extraction in faecal samples [125]. Moreover, PCR assays are very costly for diagnostic laboratory use [126] and are therefore commonly used in research.

Serodiagnosis cannot be used to differentiate between present and previous infection and is therefore not useful for the diagnosis of giardiasis.

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6. Treatment

Treatment of giardiasis in livestock is through use of fenbendazole and albendazole, which have been shown to be effective in the elimination of Giardiafrom both housed and range calves [32, 127129] as well as improving the mucosal microvillus structure and function within a week [129]. In sheep, treatment with fenbendazole at a dose of 10 mg/kg for three consecutive days, has been shown to successfully clear the infection. In an outbreak of giardiasis on a sheep farm, Giardia-infected lambs (30–90 days of age) presenting with malabsorption, decreased weight gain, and reduced feed efficiency recovered rapidly from the symptoms and poor weight gain after treatment with fenbendazole [69]. Similarly, in calves experimentally infected with G. duodenalisand treated with fenbendazole, a significant difference in weight gain was noticed between fenbendazole-treated and untreated calves. Animals in the treatment group gained on average 2.86 kg (equal to 102 g per day) more than the animals in the control group [27]. However, in some other treatment studies where fenbendazole or paromomycin sulphate were used, differences in mean body weight, average daily weight gain, or feed intake between the control and treated groups were not significant, although there was a slightly higher weight gain and lower occurrence of diarrhoea in the treated groups [12, 42].

In dogs and cats, fenbendazole is the commonly used therapy, normally given once daily for 3–5 days. Albendazole can be used but it has been associated with bone marrow suppression in both dogs and cats, and so no longer being used in both animal species [130]. Vaccines for Giardiain dogs and cats have been developed and they are reported to have the ability to reduce the duration of shedding of cysts which may subsequently reduce environmental contamination [131]. A prolonged treatment up to 5 days was shown not to be statistically better than treatment for three consecutive days [132]. On the other hand, metronidazole has been used to treat giardiasis in horses, with resolution of clinical signs after treatment [112].

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7. Conclusions

Giardiainfections are prevalent in livestock and companion animals. A number of studies have reported and genotyped Giardiain domestic animals, particularly livestock and companion animals, and have found that they may be infected with zoonotic or species-specific genotypes. However, there is still limited information on infection rates in pigs and horses. Further, the role of these animals and dogs in the zoonotic transmission of Giardiastill needs further investigation. Studies reporting the existence of zoonotic assemblages in both animals and humans in the same locality (e.g. for dogs) emphasise the need for further studies on zoonotic transmission of Giardia. Such information will assist in further highlighting the public health significance of Giardia. Increased interaction and the nature of the interaction between companion animals and their owners can determine whether zoonotic infection occurs or not.

Economic implications of the disease in terms of treatment costs that the farmers have to incur cannot be overlooked especially in livestock (particularly dairy calves). Giardiasis adversely affects production; and chronic cases may impact negatively on the performance of affected animals resulting in reduced weight gain, impaired feed efficiency and delayed maturity. These loses translate into food loses.

Unfortunately, giardiasis in humans is not a health priority in most countries but the effect of the parasite in terms of patient well-being and its effect on quality of life have been highlighted by many authors, highlighting its impact on human health.

A better understanding of the disease in animals (livestock and companion animals), the species and transmission patterns is necessary for appropriate prevention and control strategies which should result in increased livestock production and reduced treatment costs for the farmers or animal owners. More molecular epidemiological studies are required especially in areas where these have not been conducted such as sub-Saharan Africa to understand and probably be able to relate human and animal infections. Treatment of Giardiainfection in both livestock and companion animals is recommended whether or not they are clinically ill, because of the potential for zoonotic transmission.

References

  1. 1. FAO. Major Livestock Production Systems in Africa. Available from:http://www.fao.org/wairdocs/ilri/x5547e/x5547e0o.htm. [Accessed: 3 April 2017]
  2. 2. Beck AM. The impact of the canine cleanup law: Both dogs and people profit. Environment: Science and Policy for Sustainable Development. 1979;21:197. DOI: 10.1080/00139157.1979.9931200
  3. 3. Szabova E, Juris P, Miterpakova M, Antolova D, Papajova I, Sefcikova H. Prevalence of important zoonotic parasites in dog populations from the Slovak Republic. Helminthologia. 2007;44:170-176. DOI: 10.2478/s11687-007-0027-3
  4. 4. Feng Y, Xiao L. Zoonotic potential and molecular epidemiology ofGiardiaspecies and giardiasis. Clinical Microbiology Reviews. 2011;24:110-140. DOI: 10.1128/CMR.00033-10
  5. 5. Berrilli F, Di Cave D, De Liberato C, Franco A, Scaramozzino P, Orecchia P. Genotype characterisation ofGiardia duodenalisisolates from domestic and farm animals by SSU-rRNA gene sequencing. Veterinary Parasitology. 2004;122:193-199. DOI: 10.1016/j.vetpar.2004.04.008
  6. 6. Thompson RCA. The zoonotic significance and molecular epidemiology ofGiardiaand giardiasis. Veterinary Parasitology. 2004;126:15-35. DOI: 10.1016/j.vetpar.2004.09.008
  7. 7. Heyworth MF.Giardia duodenalisgenetic assemblages and hosts. Parasite. 2016;23:13. DOI: 10.1051/parasite/2016013
  8. 8. Ey PL, Mansouri M, Kulda J, Nohýnková E, Monis PT, Andrews RH, Mayrhofer G. Genetic analysis ofGiardiafrom hoofed farm animals reveals artiodactyl-specific and potentially zoonotic genotypes. Journal of Eukaryotic Microbiology. 1997;44:626-635. DOI: 10.1111/j.1550-7408.1997.tb05970.x
  9. 9. Hopkins RM, Meloni BP, Groth DM, Wetherall JD, Reynoldson JA, Thompson RCA, Ribososomal RNA. sequencing reveals differences between the genotypes ofGiardiaisolates recovered from humans and dogs in the same locality. Journal of Parasitology. 1997;83:44. DOI: 10.2307/3284315
  10. 10. Bowman DD. Georgis’ Parasitology for Veterinarians. 9th ed. Saunders Elsevier. St Louis Missouri. 2009; ISBN: 978-1-4160-4412-3
  11. 11. Lasek-Nesselquist E, Welch DM, Sogin ML. The identification of a newGiardia duodenalisassemblage in marine vertebrates and a preliminary analysis ofG. duodenalispopulation biology in marine systems. International Journal for Parasitology. 2010;40:1063-1074. DOI: 10.1016/j.ijpara.2010.02.015
  12. 12. O’Handley R, Olson M, Fraser D, Adams P, Thompson R. Prevalence and genotypic characterization ofGiardiain dairy calves from Western Australia and Western Canada. Veterinary Parasitology. 2000;90:193-200. DOI:http://dx.doi.org/10.1016/S0304-4017(00)00235-1
  13. 13. Geurden T, Geldhof P, Levecke B, Martens C, Berkvens D, Casaert S, Vercruysse J,Claerebout E. MixedGiardia duodenalisassemblage A and E infections in calves. International Journal for Parasitology. 2008;38:259-264. DOI: 10.1016/j.ijpara.2007.07.016
  14. 14. Lebbad M, Mattsson J, Christensson D, Ljungstrom B, Backhans A, Andersson J, Svard S.From mouse to moose: Multilocus genotyping ofGiardiaisolates from various animal species. Veterinary Parasitology. 2010;168:231-239. DOI: 10.1016/j.vetpar.2009.11.003
  15. 15. Mircean V, Györke A, Cozma V. Prevalence and risk factors ofGiardia duodenalisin dogs in Romania. Veterinary Parasitology. 2012;184:325-329. DOI: 10.1016/j.vetpar.2011.08.022
  16. 16. Minetti C, Taweenan W, Hogg R, Featherstone C, Randle N, Latham SM, Wastling JM.Occurrence and diversity ofGiardia duodenalisassemblages in livestock in the UK.Transboundary and Emerging Diseases. 2013;61:e60-e67. DOI: 10.1111/tbed.12075
  17. 17. Lane S, Lloyd D. Current trends in research into the waterborne parasiteGiardia. Critical Reviews in Microbiology. 2002;28:123-147. DOI: 10.1080/1040-840291046713
  18. 18. WHO. The World Health Report 1996. Fighting Disease Fostering Development. Geneva: World Health Organization; 1996
  19. 19. Olson M, O’Handley R, Ralston B, McAllister T, Thompson R. Update onCryptosporidiumandGiardiainfections in cattle. Trends in Parasitology. 2004;20:151-198. DOI: 10.1016/j.pt.2004.01.015
  20. 20. Thompson R, Monis P.Giardia –from genome to proteome. Advances in Parasitology. 2012;78:57-95. DOI:http://dx.doi.org/10.1016/B978-0-12-394303-3.00003-7
  21. 21. Gow S, Waldner C. An examination of the prevalence of and risk factors for shedding ofCryptosporidiumspp. andGiardiaspp. in cows and calves from western Canadian cow-calf herds. Veterinary Parasitology. 2006;137:50-61. DOI: 10.1016/j.vetpar.2005.05.071
  22. 22. Hamnes I, Gjerde B, Robertson L. Prevalence ofGiardiaandCryptosporidiumin dairy calves in three areas of Norway. Veterinary Parasitology, 2006;140:204-216. DOI:http://dx.doi.org/10.1016/j.vetpar.2006.03.024
  23. 23. Graczyk TK, Grimes BH, Knight R, Da Silva AJ, Pieniazek NJ, Veal DA. Detection ofCryptosporidiumparvum andGiardia lambliacarried by synanthropic flies by combined fluorescent in situ hybridization and a monoclonal antibody. American Journal of Tropical Medicine and Hygiene. 2003;68:228-232. DOI:https://doi.org/10.4269/ajtmh.2003.68.228
  24. 24. Rendtorff RC. The experimental transmission of human intestinal protozoan parasites. II.Giardia lambliacysts given in capsules. American Journal of Hygiene. 1954;59:209-220. PMID: 13138586 ISSN: 0096-5294
  25. 25. Faubert GM. The immune response toGiardia. Parasitology Today. 1996;12:140-145. DOI:https://doi.org/10.1016/0169-4758(96)10004-1
  26. 26. Buret AG. Pathophysiology of enteric infections withGiardia duodenalis. Parasite. 2008;15:261-265. DOI:https://doi.org/10.1051/parasite/2008153261
  27. 27. Geurden T, Vandenhoute E, Pohle H, Casaert S, De Wilde N, Vercruysse J, Claerebout E. The effect of a fenbendazole treatment on cyst excretion and weight gain in calves experimentally infected withGiardia duodenalis. Veterinary Parasitology. 2010;169:18-23. DOI:http://dx.doi.org/10.1016/j.vetpar.2009.12.027
  28. 28. Koh W, Geurden T, Paget T, O’Handley R, Steuart R, Thompson R, Buret A.Giardia duodenalisassemblage-specific induction of apoptosis and tight junction disruption in human intestinal epithelial cells: Effects of mixed infections. Journal of Parasitology. 2013;99:353-358. doi:http://dx.doi.org/10.1645/GE-3021.1
  29. 29. McDonnell P, Scott K, Teoh D, Olson M, Upcroft J, Upcroft P, Buret A.Giardia duodenalistrophozoites isolated from a parrot (Cacatua galerita) colonize the intestinal tracts of domestic kittens and lambs. Veterinary Parasitology. 2002;111:31-46. DOI:http://dx.doi.org/10.1016/S0304-4017(02)00349-7
  30. 30. Scott KG, Meddings JB, Kirk DR, Lees-Miller SP, Buret AG. Intestinal infection withGiardiaspp. reduces epithelial barrier function in a myosin light chain kinase-dependent fashion. Gastroenterology 2002;123:1179-1190. DOI:http://dx.doi.org/10.1053/gast.2002.36002
  31. 31. Buret AG. Mechanisms of epithelial dysfunction in giardiasis. Gut 2007;56:328-335. DOI:http://dx.doi.org/10.1136/gut.2006.107771
  32. 32. O’Handley M, Buret A, McAllister T, Jelinski M, Olson M. Giardiasis in dairy calves: effects of fenbendazole treatment on intestinal structure and function. International Journal for Parasitology 2001;31:73-79. DOI:http://dx.doi.org/10.1016/S0020-7519(00)00148-X
  33. 33. Kahn C, Line S. The Merck Veterinary Manual. Merck and Company Inc. New Jersey, USA. Giardiasis; 2010; pp. 190-192; 170. ISBN-13: 978-0911910933; ISBN-10: 091191093X
  34. 34. Chin HS, Palm D, McArthur AG, Svärd SG, Gillin FD. A novel Myb-related protein involved in transcriptional activation of encystation genes inGiardia lamblia. Clinical Microbiology. 2002;46:971-984. DOI: 10.1046/j.1365-2958.2002.03233.x
  35. 35. Eckmann L. Mucosal defenses againstGiardia. Parasite Immunology. 2003;25:259-270. DOI: 10.1046/j.1365-3024.2003.00634.x
  36. 36. O’Handley R, Cockwill C, McAllister T, Jelinski M, Morck D, Olson M. Duration of naturally acquired giardiosis and cryptosporidiosis in dairy calves and their association with diarrhoea. Journal of the American Veterinary Medical Association. 1999;214:391-396 10023403
  37. 37. Ralston B, McAllister T, Olson M. Prevalence and infection pattern of naturally acquired giardiasis and cryptosporidiosis in range beef calves and their dams. Veterinary Parasitology. 2003;114:113-122. DOI:http://dx.doi.org/10.1016/S0304-4017(03)00134-1
  38. 38. Xiao L, Herd RP. Epidemiology of equineCryptosporidiumandGiardiainfections. Equine Veterinary Journal. 1994;26:14-17. DOI: 10.1111/j.2042-3306.1994.tb04323.x
  39. 39. Becher K, Robertson I, Fraser D, Palmer D, Thompson R. Molecular epidemiology ofGiardiaandCryptosporidiuminfections in dairy calves originating from three sources in Western Australia. Veterinary Parasitology. 2004;123:19. DOI:http://dx.doi.org/10.1016/j.vetpar.2004.05.020
  40. 40. Appelbee A, Thompson R, Olson E.GiardiaandCryptosporidiumin mammalian wildlife-current status and future needs. Trends in Parasitology. 2005;21:370-376. DOI:http://dx.doi.org/10.1016/j.pt.2005.06.004
  41. 41. Thompson RC, Carlysle S, Palmer CS, O’Handley, R. The public health and clinical significance ofGiardiaandCryptosporidiumin domestic animals. The Veterinary Journal. 2008;177:18-25. DOI:http://dx.doi.org/10.1016/j.tvjl.2007.09.022
  42. 42. Geurden T, Claerebout E, Dursin L, Deflandre A, Bernay F, Kaltsatos V, Vercruysse J.The efficacy of an oral treatment with paromomycin against an experimental infection withGiardiain calves. Veterinary Parasitology. 2006;135:241247. DOI:http://dx.doi.org/10.1016/j.vetpar.2005.09.006
  43. 43. Olson M, McAllister T, Deselliers L, Morck D, Cheng K, Buret A, Ceri H. Effects of giardiasis on production in a domestic ruminant (lamb) model. American Journal of Veterinary Research. 1995;56:1470-1474 8585658
  44. 44. Huetink R, van der Giessen J, Noordhuizen J, Ploeger H. Epidemiology ofCryptosporidiumspp. andGiardia duodenalison a dairy farm. Veterinary Parasitology. 2001;102:53-67. DOI:http://dx.doi.org/10.1016/S0304-4017(01)00514-3
  45. 45. Xiao L.Giardiainfection in farm animals. Parasitology Today 1994;10:436-438. DOI:https://doi.org/10.1016/0169-4758(94)90178-3
  46. 46. O’Handley RM.Giardiain farm animals. In: Olson BE, Olson ME, Wallis PM, editors.Giardia: The Cosmopolitan Parasite. Wallingford, UK: CAB International; 2002. p. 97-105
  47. 47. Sabry M, Taher E, Meabed E. Prevalence and genotyping of zoonoticGiardiafrom Fayoum Governorate, Egypt. Research Journal of Parasitology. 2009;4:105-114. ISSN: 1816-4943
  48. 48. Di Cristanziano V, Santoro M, Parasi F, Albonico M, Shaali M, Di Cave D, Berrilli F. Genetic characterization ofGiardia duodenalisby sequence analysis in humans and animals in Pemba Island, Tanzania. Parasitology International 2013;63:438-441. DOI:http://dx.doi.org/10.1016/j.parint.2013.11.004
  49. 49. Helmy YA, Krücken J, Nöckler K, Samson-Himmelstjerna G, Zessin GH. Comparison between two commercially available serological tests and polymerase chain reaction in the diagnosis ofCryptosporidiumin animals and diarrhoeic children. Parasitology Research. 2014;113:211. DOI: 10.1007/s00436-013-3645-3
  50. 50. Kakandelwa C, Siwila J, Nalubamba KS, Muma JB, Phiri IGK. Prevalence ofGiardiain dairy cattle in Lusaka and Chilanga districts, Zambia. Veterinary Parasitology. 2016;215:114-116. DOI:http://dx.doi.org/10.1016/j.vetpar.2015.11.004
  51. 51. Trout J, Santı’n M, Greiner E, Fayer R. Prevalence and genotypes ofGiardia duodenalisin post-weaned dairy calves. Veterinary Parasitology. 2005;130:177-183. DOI:http://dx.doi.org/10.1016/j.vetpar.2005.03.032
  52. 52. Mendonca C, Almeida A, Castro A, de Lurdes Delgado M, Soares S, da Costa, M, et al. Molecular characterization ofCryptosporidiumandGiardiaisolates from cattle from Portugal. Veterinary Parasitology 2007;147:47-50. DOI:http://dx.doi.org/10.1016/j.vetpar.2007.03.019
  53. 53. Monis T, Andrews H, Mayrhofer G, Ey L. Genetic diversity within the morphological speciesGiardia intestinalisand its relationship to host origin. Infection, Genetics and Evolution. 2003;3:29-38. DOI:http://dx.doi.org/10.1016/S1567-1348(02)00149-1.
  54. 54. Thompson RC, Monis PT. Variation inGiardia: Implications for taxonomy and epidemiology. Advances in Parasitology. 2004;58: 69-137. DOI:http://dx.doi.org/10.1016/S0065-308X(04)58002-8
  55. 55. Sischo WM, Atwill ER, Lanyon LE, George J. Cryptosporidia on dairy farms and the role that these farms may have in contaminating surface water supplies in the Northeastern United States. Preventive Veterinary Medicine, 2000;43:253-267. DOI:http://dx.doi.org/10.1016/S0167-5877(99)00107-5
  56. 56. Ryan UM, Bath C, Robertson I, Read C, Elliot A, McInnes L, Traub R, Besier B. Sheep may not be an important zoonotic reservoir forCryptosporidiumandGiardiaparasites. Applied Environmental Microbiology. 2005;71:4992-4997. DOI: 10.1128/AEM.71.9.4992-4997.2005
  57. 57. Castro-Hermida JA, Almeid A, Gonzalez-Warleta M, Da Costa JM, Mezo M. Prevalence and preliminary genetic analysis ofGiardiaisolated from adult sheep in Galicia (northwest Spain). Journal of Eukaryotic Microbiology. 2006;53(Suppl 1):S172-S173. DOI: 10.1111/j.1550-7408.2006.00220.x
  58. 58. Castro-Hermida JA, Almeida A, Gonzalez-Warleta M, Correia da Costa JM, Rumbo Lorenzo C, Mezo M. Occurrence ofCryptosporidium parvumandGiardia duodenalisin healthy adult domestic ruminants. Parasitology Research. 2007;101:1443-1448. DOI: 10.1007/s00436-007-0624-6
  59. 59. Santı’n M, Trout JM, Fayer R. Prevalence and molecular characterization ofCryptosporidiumandGiardiaspecies and genotypes in sheep in Maryland. Veterinary Parasitology. 2007;146:17-24. DOI:http://dx.doi.org/10.1016/j.vetpar.2007.01.010
  60. 60. Wegayehu T, MdR K, Li J, Adamu H, Erko B, Zhang L, Tilahun G. Prevalence and genetic characterization ofCryptosporidiumspecies andGiardia duodenalisin lambs in Oromia Special Zone, Central Ethiopia. BMC Veterinary Research. 2017;13:22. DOI: 10.1186/s12917-016-0916-0
  61. 61. Wang H, Qi M, Zhang K, Li J, Huang J, Ning C, Zhang L. Prevalence and genotyping ofGiardia duodenalisisolated from sheep in Henan Province, central China. Infection, Genetics and Evolution. 2016;39:330-335. DOI:http://dx.doi.org/10.1016/j.meegid.2016.02.006
  62. 62. Olson M, Thorlakson C, Deselliers L, Morck D, McAllister T.GiardiaandCryptosporidiumin Canadian farm animals. Veterinary Parasitology, 1997;68,375-381. DOI:http://dx.doi.org/10.1016/S0304-4017(96)01072-2
  63. 63. Paz e Silva FM, Lopes RS, Bresciani KDS, Amarante AFT, Araujo JP Jr. High occurrence ofCryptosporidium ubiquitumandGiardia duodenalisgenotype E in sheep from Brazil. Acta Parasitologica. 2014;59:193-196. DOI: 10.2478/s11686-014-0223-5
  64. 64. Ye J, Xiao L, Wang Y, Guo Y, Roellig DM, Feng Y. Dominance ofGiardia duodenalisassemblage A and Enterocytozoon bieneusi genotype BEB6 in sheep in Inner Mongolia, China. Veterinary Parasitology 2015;210:235-239. DOI:http://dx.doi.org/10.1016/j.vetpar.2015.04.011
  65. 65. Yang R, Jacobson C, Gordon C, Ryan U. Prevalence and molecular characterization ofCryptosporidiumandGiardiaspecies in pre-weaned sheep in Australia. Veterinary Parasitology 2009;161:19-24. DOI:http://dx.doi.org/10.1016/j.vetpar.2008.12.021
  66. 66. Giangaspero A, Paoletti B, Iorio R, Traversa D. Prevalence and molecular characterization ofGiardia duodenalisfrom sheep in central Italy. Parasitology Research. 2005;96:32-37. DOI: 10.1007/s00436-005-1317-7
  67. 67. Geurden T, Thomas P, Casaert S, Vercruysse J, Claerebout E. Prevalence and molecular characterization ofCryptosporidiumandGiardiain lambs and goat kids in Belgium. Veterinary Parasitology. 2008;155:142-145. DOI:http://dx.doi.org/10.1016/j.vetpar.2008.05.002
  68. 68. Van der Giessen JW, de Vries A, Roos M, Wielinga P, Kortbeek LM, Mank TG. Genotyping ofGiardiain Dutch patients and animals: A phylogenetic analysis of human and animal isolates. International Journal of Parasitology 2006;36:849-858. DOI: 10.1016/j.ijpara.2006.03.001
  69. 69. Aloisio F, Filippini G, Antenucci P, Lepri E, Pezzotti G, Caccio SM, Pozio E. Severe weight loss in lambs infected withGiardia duodenalisassemblage B. Veterinary Parasitology. 2006;142:154-158. DOI: 10.1016/j.vetpar.2006.06.023
  70. 70. Appelbee AJ, Frederick LM, Heitman TL, Olson ME. Prevalence and genotyping ofGiardia duodenalisfrom beef calves in Alberta, Canada. 2003;112:289-294. DOI:http://dx.doi.org/10.1016/S0304-4017(02)00422-3
  71. 71. Ruiz A, Foronda P, Gonzalez JF, Guedes A, Abreu-Acosta N, Molina JM, Valladares B. Occurrence and genotype characterization ofGiardia duodenalisin goat kids from the Canary Islands, Spain. Veterinary Parasitology. 2008;154:137-141. DOI:http://dx.doi.org/10.1016/j.vetpar.2008.03.003
  72. 72. Berilli F, D’Alfonso R, Giangaspero A, Marangi M, Brandonisio O, Kabore Y, Gle C, Cianfanelli C, Lauro R, Cave D.Giardia duodenalisgenotypes andCryptosporidiumspecies in humans and domestic animals in Côte dÍvoire: Occurrence and evidence for environmental contamination. Transactions of the Royal Society of Tropical Medicine and Hygiene. 2012;106:191-195. DOI:http://dx.doi.org/10.1016/j.trstmh.2011.12.005
  73. 73. Lim YAL, Mahdy MAK, Tan TK, Goh XT, Jex AR, Nolan MJ, Sharma RSK, Gasser RB. First molecular characterization ofGiardia duodenalisfrom goats in Malaysia. Molecular and Cellular Probes 2013;27:28-31. DOI:http://dx.doi.org/10.1016/j.mcp.2012.08.006
  74. 74. Akinkuotu OA, Okwelum N, Famakinde SA, Akinkuotu AC, Oseni OT.Giardiainfection in recently acclimatized kalahari red goats in Nigeria. Nigerian Veterinary Journal. 2016;37:16-23 ISSN 0331-3026
  75. 75. Robertson LJ.GiardiaandCryptosporidiuminfections in sheep and goats: A review of the potential for transmission to humans via environmental contamination. Epidemiology and Infection. 2009;137:913-921. DOI: 10.1017/S0950268809002295
  76. 76. Gomez-Munoz MT, Navarro C, Garijo-Toledo MM, Dea-Ayuela MA, Fernandez-Barredo S, Perez-Gracia MT, Dominguez-Marquez MV, Borras R. Occurrence and genotypes ofGiardiaisolated from lambs in Spain. Parasitology International 2009;58:297-299. DOI:http://dx.doi.org/10.1016/j.parint.2009.06.005
  77. 77. Zhang W, Zhang X, Wang R, Liu A, Shen Y, Ling H, Cao J, Yang F, Zhang X, Zhang L. Genetic characterizations ofGiardia duodenalisin sheep and goats in Heilongjiang Province, China and possibility of zoonotic transmission. PLoS Neglected Tropical Disease. 2012;6:e1826. DOI:http://dx.doi.org/10.1371/journal.pntd.0001826
  78. 78. Sanford SE. Enteric cryptosporidial infection in pigs: 184 cases (1981-1985). Journal of the American Veterinary Medical Association. 1987;190:695-698. PMID:3570923
  79. 79. Koudela B, Nohynkova E, Vitovec J, Pakandl M, Kulda J.Giardiainfections in pigs: Detection and in vitro isolation if trophozoites of theGiardia intestinalisgroup. Parasitology 1991;102:163-166. DOI:http://dx.doi.org/10.1017/S0031182000062442
  80. 80. Xiao L, Herd RP, Bowman GL. Prevalence ofCryptosporidiumandGiardiainfections on two Ohio pig farms with different management systems. Veterinary Parasitology. 1994;52: 331-336. DOI:http://dx.doi.org/10.1016/0304-4017(94)90124-4
  81. 81. Atwill ER, Sweitzer RA, Pereira MG, Gardner IA, Van Vuren D, Boyce WM. Prevalence of and associated risk factors for sheddingCryptosporidium parvumoocysts andGiardiacysts within feral pig populations in California. Applied and Environmental Microbiology. 1997;63:3946-3949 0099-2240/97/$04.0010. ISSN: 1098-5336
  82. 82. Farzan A, Parrington L, Coklin T, Cook A, Pintar K, Pollari F, Friendship R, Farber J, Dixon B. Detection and characterization ofGiardia duodenalisandCryptosporidiumspp. on swine farms in Ontario, Canada. Foodborne Pathogens and Disease. 2011;8:1207-1213
  83. 83. Maddox-Hyttel C, Langkjaer RB, Enemark HL, Vigre H.CryptosporidiumandGiardiain different age groups of Danish cattle and pigs – Occurrence and management of associated risk factors. Veterinary Parasitology. 2006;141:48-59http://dx.doi.org/10.1016/j.vetpar.2006.04.032, PMID: 16797848
  84. 84. Hamnes I, Gjerde B, Forberg T, Robertson L. Occurrence ofCryptosporidiumandGiardiain suckling piglets in Norway. Veterinary Parasitology. 2007;144:222-233. DOI:http://dx.doi.org/10.1016/j.vetpar.2006.10.011
  85. 85. Langkjaer RB, Vigre H, Enemark HL, Maddox-Hyttel C. Molecular and phylogenetic characterization ofCryptosporidiumandGiardiafrom pigs and cattle in Denmark. Parasitology. 2007;134:339-350. DOI: 10.1017/S0031182006001533
  86. 86. Siwila J, Mwape KE. Prevalence ofCryptosporidiumspp. andGiardia duodenalisin pigs in Lusaka, Zambia. Onderstepoort Journal of Veterinary Research. 2012;79:5 pages, Art. #404. DOI:http://dx.doi.org/10.4102/ojvr.v79i1.404
  87. 87. Armson A, Yang R, Thompson J, Johnson J, Reid S, Ryan UM.Giardiagenotypes in pigs in Western Australia: prevalence and association with diarrhoea. Experimental Parasitology. 2009;121:381-383. DOI: 10.1016/j.exppara.2009.01.008
  88. 88. Sprong H, Caccio SM, van der Giessen JW. Identification of zoonotic genotypes ofGiardia duodenalis. PLoS Neglected Tropical Diseases. 2009;3:e558. DOI:http://dx.doi.org/10.1371/journal.pntd.0000558
  89. 89. Xiao L, Fayer R. Molecular characterisation of species and genotypes ofCryptosporidiumandGiardiaand assessment of zoonotic transmission. International Journal of Parasitology 2008;38:1239-1255. DOI:http://dx.doi.org/10.1016/j.ijpara.2008.03.006
  90. 90. Traub RJ. The veterinary public health significance ofGiardiaandCryptosporidium: getting things in perspective. Veterinary Journal. 2008;177:309-310. DOI: 10.1016/j.tvjl.2008.06.013
  91. 91. Claerebout E, Casaert S, Dalemans AC, De Wilde N, Levecke B, Vercruysse J, Geurden T.Giardiaand other intestinal parasites in different dog populations in Northern Belgium. Veterinary Parasitology. 2009;161:41-46. DOI:http://dx.doi.org/10.1016/j.vetpar.2008.11.024
  92. 92. Bouzid M, Halai K, Jeffreys D, Hunter PR. The prevalence ofGiardiainfection in dogs and cats: a systematic review and meta-analysis of prevalence studies from stool samples. Veterinary Parasitology. 2015;207:181-202. DOI: 10.1016/j.vetpar.2014.12.011
  93. 93. Stehr-Green JK, Murray G, Schantz PM, Wahlquist SP. Intestinal parasites in pet store puppies in Atlanta. American Journal of Public Health. 1987;77:345-346. DOI: 10.2105/AJPH.77.3.345
  94. 94. Papini G, Gorini A, Spaziani R, Cardini G. Survey on giardiasis in shelter dog populations. Veterinary Parasitology. 2005;128:333-339. DOI:http://dx.doi.org/10.1016/j.vetpar.2004.12.005
  95. 95. Dubná S, Langrova J, Napravnik I, Jankovska J, Vadlejch Pekar S, Fechtner J. The prevalence of intestinal parasites in dogs from Prague, rural areas, and shelters of the Czech Republic. Veterinary Parasitology. 2007;145:120-128. DOI:http://dx.doi.org/10.1016/j.vetpar.2006.11.006
  96. 96. Mark-Carew MP, Adesiyun AA, Basu A, Georges KA, Pierre T, Tilitz S, Wade SE, Mohammed HO. Characterization ofGiardia duodenalisinfections in dogs in Trinidad and Tobago. Veterinary Parasitology. 2013;196:199-202. DOI:http://dx.doi.org/10.1016/j.vetpar.2013.01.023
  97. 97. Bugg RJ, Robertson ID, Elliot AD, Thompson RCA. Gastrointestinal parasites of urban dogs in Perth, Western Australia. Veterinary Journal. 1999;157:295-301. DOI:https://doi.org/10.1053/tvjl.1998.0327
  98. 98. McGlade TR, Robertson ID, Elliott AD, Thompson RCA. High prevalence ofGiardiadetected in cats by PCR. Veterinary Parasitology. 2003;110:197-205. DOI:http://dx.doi.org/10.1016/S0304-4017(02)00322-9
  99. 99. Thompson RCA, Robertson ID. Gastrointestinal parasites of dogs and cats: current issues. Compendium on continuing education for the practising. The Veterinarian. 2003;25:4-11
  100. 100. Ballweber LR, Xiao L, Bowman DD, Kahn G, Cama VA. Giardiasis in dogs and cats: update on epidemiology and public health significance. Trends in Parasitology. 2010;26:180-189. DOI:http://dx.doi.org/10.1016/j.pt.2010.02.005
  101. 101. Traub RJ, Monis P, Robertson I, Irwin P, Mencke N, Thompson RCA. Epidemiological and molecular evidence supports the zoonotic transmission ofGiardiaamong humans and dogs living in the same community. Parasitology. 2004;128:253-262. DOI: 10.1017/S0031182003004505
  102. 102. Volotao AC, Costa-Macedo L M, Haddad FS, Brandao A, Peralta JM, Fernandes O. Genotyping ofGiardia duodenalisfrom human and animal samples from Brazil using beta-giardin gene: A phylogenetic analysis. Acta Tropica 2007;102:10-19. DOI:http://dx.doi.org/10.1016/j.actatropica.2007.02.010
  103. 103. Traub R, Inpankaew T, Reid S, Sutthikornchai C, Sukthana Y, Robertson I, Thompson R. Transmission cycles ofGiardia duodenalisin dogs and humans in Temple communities of Bangkok – A critical evaluation of its prevalence using three diagnostic tests in the field in the absence of a gold standard. Acta Tropica. 2009;111:125132. DOI:http://dx.doi.org/10.1016/j.actatropica.2007.02.010
  104. 104. Covacin C, Aucoin DP, Elliot A, Thompson RC. Genotypic characterisation ofGiardiafrom domestic dogs in the USA. VeterinaryParasitology. 2011;177:2832. DOI:http://dx.doi.org/10.1016/j.vetpar.2010.11.029
  105. 105. Farthing MJG. Giardiasis as a disease. In: Thompson RCA, Reynoldson JA, Lymbery AJ, editors.Giardia: From Molecules to Disease. Wallingford, England: CAB International; 1994. pp. 15-37
  106. 106. Robertson ID, Irwin PJ, Lymbery AJ, Thompson RCA. The role of companion animals in the emergence of parasitic zoonoses’, International Journal of Parasitology. 2000;30:13691377. DOI:http://dx.doi.org/10.1016/S0020 7519(00)00134-X
  107. 107. Fantham HB. Some parasitic protozoa found in South Africa: IV. South African Journal of Science. 1921;18:164170. ISSN: 0038-2353
  108. 108. Bemrick W.Giardiain North American horses. Veterinary Medicine Small Animal Clinics. 1968;63:163-165. PMID:5185280
  109. 109. Atwill ER, McDougald NK, Perea L. Cross-sectional study of faecal shedding ofGiardia duodenalisandCryptosporidium parvumamong packstock in the Sierra Nevada Range. Equine Veterinary Journal. 2000;32:247-252. DOI: 10.2746/042516400776563545
  110. 110. Veronesi F, Passamonti F, Caccio S, Diaferia M, Fioretti DP. Epidemiological survey on equineCryptosporidiumandGiardiainfections in Italy and molecular characterization of isolates. Zoonoses and Public Health. 2010;57:510-517. DOI: 10.1111/j.1863-2378.2009.01261.x
  111. 111. Manahan FF. Diarrhoea in horses with particular reference to a chronic diarrhoea syndrome. Australian Veterinary Journal. 1970;46:231-234. DOI: 10.1111/j.1751-0813.1970.tb02014.x
  112. 112. Kirkpatrick CE, Skand DL. Giardiasis in a horse. Journal of the American Veterinary Medical Association. 1985;187:163-164. PMID:4030452
  113. 113. Pavlásek I, Hess L, Stehlik I, Stika V. The first detection ofGiardiaspp. in horses in the Czech Republic. Veterinární Medicína. 1995;40:81-86. PMID:7762123
  114. 114. Beelitz P, Göbel E, Gothe R. Spectrum of species and incidence of endoparasites in foals and their mother mares from breeding farms with and without anthelmintic prophylaxis in upper Bavaria. Tierarztliche Praxis. 1996;24:48-54. PMID: 8720956 (Abstract)
  115. 115. Johnson E, Atwill ER, Filkins ME, Kalush J. The prevalence of shedding ofCryptosporidiumandGiardiaspp. based on a single fecal sample collection from each of 91 horses used for backcountry recreation. Journal of Veterinary Diagnostic Investigation. 1997;9:56-60
  116. 116. Traub R, Wade S, Read C, Thompson A, Mohammed H. Molecular characterization of potentially zoonotic isolates ofGiardia duodenalisin horses. Veterinary Parasitology 2005;130:317-321. DOI:http://dx.doi.org/10.1016/j.vetpar.2005.02.011
  117. 117. Traversa D, Otranto D, Milillo P, Latrofa MS, Giangaspero A, Di Cesare A, Paoletti B.Giardia duodenalissub-Assemblage of animal and human origin in horses. Infection, Genetics and Evolution 2012;12:1642-1646. DOI:http://dx.doi.org/10.1016/j.meegid.2012.06.014
  118. 118. Monis PT, Andrews RH, Mayrhofer G, Ey PL. Molecular systematics of the parasitic protozoanGiardia intestinalis. Molecular Biology and Evolution. 1999;16:1135-1144. DOI:https://doi.org/10.1093/oxfordjournals.molbev.a026204
  119. 119. Zajac AM, Johnson J, King SE. Evaluation of the importance of centrifugation as a component of zinc sulfate fecal flotation examinations. Journal of American Animal Hospital Association. 2002;38:221-224. DOI:http://dx.doi.org/10.5326/0380221
  120. 120. Garcia LS. Diagnostic Medical Parasitology. 5th ed. Washington, DC: ASM press; 2007. pp. 813-816
  121. 121. Addis DG, Mathews HM, Stewart JM, Walquist SP, Williams RM, Finton RJ, Spencer HC, Juranek DD. Evaluation of a commercially available enzyme linked immunosorbent assay forGiardia lambliaantigen in stool. Journal of Clinical Microbiology. 1991;29:1137-1142 0095-1137/91/061137-06$02.00/0. PMCID: PMC269958
  122. 122. Farthing MJG. Giardiasis. In: Gills HM, editor. Edns Protozoal Diseases. UK: Arnold Publishers; 1999. p. 562-584
  123. 123. Tangtrongsup S. Update on the diagnosis and management ofGiardiaspp infections in dogs and cats. Topics in Companion Animal Medicine. 2010;25:155-162. DOI: 10.1053/j.tcam.2010.07.003
  124. 124. Caccio S, De Giacomo M, Pozio E. Sequence analysis of the b-giardin gene and development of a polymerase chain reaction-restriction fragment length polymorphism assay to genotypeGiardia duodenaliscysts from human faecal samples. International Journal for Parasitology 2002;32:1023-1030. DOI:http://dx.doi.org/10.1016/S0020-7519(02)00068-1
  125. 125. Chalmers RM. Advances in diagnosis: Is microscopy still the benchmark? In: Ortega-Pierres G, Caccio S, Fayer R, Mank TG, Smith HV, Thompson RCA, editors.GiardiaandCryptosporidium, from molecules to disease. CAB International. 2009; pp. 147-157. ISBN: 13:978 1 84593 391 3
  126. 126. Savioli L, Smith H, Thompson A.GiardiaandCryptosporidiumjoin the ‘Neglected Diseases Initiative’. Trends in Parasitology. 2006;22:203-208. DOI:http://dx.doi.org/10.1016/j.pt.2006.02.015
  127. 127. Xiao L, Saeed K, Herd RP. Efficacy of albendazole and fenbendazole againstGiardiainfection in cattle. Veterinary Parasitology. 1996;61:165. DOI:https://doi.org/10.1016/0304-4017(95)00802-0
  128. 128. Garossino KC, Ralston BJ, McAllister TA, Milligan DN, Royan G, Olson ME. Individual intake and antiparasitic efficacy of free choice mineral and fenbendazole in range calves. Veterinary Parasitology. 2001;94:151. DOI:http://dx.doi.org/10.1016/S0304-4017(00)00380-0
  129. 129. O’Handley R M, Cockwill C, Jelinski M, McAllister TA, Olson ME. Effects of repeat fenbendazole treatment in dairy calves with giardiosis on cyst excretion, clinical signs and production. Veterinary Parasitology. 2000;89:209-218. DOI:http://dx.doi.org/10.1016/S0304-4017(00)00200-4
  130. 130. Stokol T, Randolph JF, Nachbar S, Rodi C, Barr SC. Development of bone marrow toxicosis after albendazole administration in a dog and cat. Journal American Veterinary Medical Association. 1997;210:1753-1756 9187723
  131. 131. Olson ME, Ceri H, Morck DW.Giardiavaccination. Parasitology Today. 2000;16:213-217. DOI:http://dx.doi.org/10.1016/S0169-4758(99)01623-3
  132. 132. Montoya A, Dado D, Mateo M, Espinosa C, Miró G. Efficacy of Drontal®flavour Plus (50 mg praziquantel 144 mg pyrantel embonate, 150 mg febantelper tablet) againstGiardiasp. in naturally infected dogs. Parasitology Research. 2008;103:1141-1144. DOI: 10.1007/s00436-008-1107-0

Written By

Joyce Siwila

Submitted: September 23rd, 2016 Reviewed: September 7th, 2017 Published: December 13th, 2017