Symptomatic Assessment of Human Giardiasis in Basrah

Background: Giardia was single celled microscopic protozoan parasites that cause enteric disease in human. It was recognized as the most common parasitological cause of diarrhea in human patients and is a major concern to drinking water authorities, as it is a frequently diagnosed waterborne infection. 
Aim: To asses symptomatically human giardiasis in Basrah population. 
Materials and Methods: This work was conducted from September 2012 to May 2013. A total 1344 stool samples were collected from human cases. 
Results: About 405 cases of human giardiasis were diagnosed out from 1344 patients. The percentages of each symptoms are as follow diarrhea 75%; foul smelling greasy stool 31.8%; bloating 22%; abdominal crump 85%; anorexia 6.4%; fever 25%; vomiting 9% and constipation 16%. 
Conclusion: Clinical examination data in human showen variety of presentation among symptoms and signs.


Introduction
Antony Van Leeuwenhoek was the first one described Giardia in his own stool in 1681 [1]. The World Health Organization added Giardia to the list of parasitic diseases in 1981 [2,3]. G. lamblia was a worldwide health problem that requires better solutions, it was the causative agent of giardiasis, a disease which affected over 200 million people per year in 2002 [4][5][6]. Giardiasis was the most frequently diagnosed water borne disease and the major public health concern of water utilities in the developed and developing nations, water is an important vehicle for the transmission of Giardia to human and livestock [7]. The life cycle of G. duodenalis comprises two main stages: a trophozoite stage which colonizes the intestinal epithelium of the host and causes disease, and an infectious cyst stage which is resistant in the environment [8]. G. duodenalis trophozoites have been reported to rarely invade the mucosa of the duodenum and jejunum, but normally they are considered non-invasive and attach to the microvillous and baso-lateral membranes of the enterocyte [9][10][11]. In addition, the normal villus structure is affected in some patients like in villus blunting (atrophy) and crypt cell hypertrophy and increases of crypt depth [12]. The colonization of trophozoites in the small intestine results in a reduction in the height of the microvilli and therefore a loss of absorptive surface area [9]. This loss of absorptive surface leads to mal-absorption of glucose, electrolytes and water, with reduces disaccharidase activity [13]. This results in the small intestine filling with mucous and fluid, and ultimately mal-digestion and hypermotility, all responsible for the clinical manifestation of diarrhea [14]. As a result, enterocytic brush border is damaged, the increased epithelial permeability leads to an inflammatory response, digestive and absorptive changes, that correlate with the brush border injury and disaccharidase deficiencies [15]. It also triggers apoptosis causing loss of epithelium barrier function with a subsequent increase in permeability [16]. It is established that the increased intestinal permeability could also result from increased luminal antigens, this could provoke the appearance of allergic reactions-a complication, often observed in humans infected with Giardia [15,17,18]. There are three types of giardiasis the asymptomatic, acute, and chronic infections [19]. Asymptomatic infection occurs in human adult and children, and other mammalian hosts and is probably the most common form of giardiasis [19,20]. Factors such as variation in parasite virulence and host immune defense may contribute to asymptomatic giardiasis [21]. The clinical manifestations of human giardiasis are individual and depend on various factors such as the route of infection, the duration of infection and the physiological condition of the host and probably, parasitic factors [12]. The acute stage generally begins with intestinal troubles, colic, followed by nausea and anorexia, early signs could be low-degree fever and lethargy. Later symptoms include profuse, watery, foul-smelling diarrhea, meteorism and enhanced peristalsis with extensive flatulence, eructation and bad taste, epigastric cramping. Rarely, feces could contain mucus or blood [22]. Although some acute episodes of giardiasis could resolve spontaneously, they usually pass into a subacute or chronic stage [23]. During the chronic stage, lethargy, headache and muscle pain with progressive weight loss, loss of appetite and mal-absorption could be present [24]. Chronic disease is often dominated by symptoms of mal-absorption [22].

Materials and Methods
About 1344 stool samples were collected from human cases for different age, sex, address, economic state and service level, during period from 10 September 2012 to 30 May 2013.

Questionnaires sheet
The patient's name: Medicine -University of Basrah for confirmed diagnosis. We used a Questionnaires sheet by which take a carful history from each case. The sheet consists of detailed location, level of services, social, clinical, environmental and source of water supply about every patient examined.

Direct smear with normal saline
Comminute 5-6 stool or faecal balls or 2-4 gm with pestle and mortar.
Transfer a loop-fall of the material to a slide matchstick, and a drop of diluted fluid (normal saline) were placed on glass microscopic slide to form a uniform suspension.
Spread it on the slide and apply cover slip.

Direct smear with Lugol′s iodine (Himedia/India)
After prepare the direct smear, used Lugol′s iodine to kill and staining the trophozoites and cysts. Adding of one drop of Lugol′s iodine to prepared slide and examination by light microscope under, low (10X) and high power (40X) according [25].

Results
405 cases of human giardiasis were diagnosed out from 1344 patients. Symptoms and sings varied from diarrhea, Foul smelling greasy stool (steatorrhea), abdominal crump, bloating, fever, anorexia, constipation and vomiting, there number of cases examined list in Table 1 below.

Discussion
In this work recorded symptomatic human giardiasis cases, this as a resulting from examined all human cases were obtained from peoples suffering from different clinical features attended to hospitals and health centers for treatment. These were agreeing with most studies like the infection with G. lamblia ranges from asymptomatic passage of cysts, to acute diarrhea, to a syndrome of chronic diarrhea and malabsorption [27]. There are two types of giardiasis: the asymptomatic and symptomatic infections [19].
The clinical picture of giardiasis varies ranging from asymptomatic infection or acute self-limiting to severe, chronic one [28]. Many factors such as variation in parasite virulence and host immune defense may contribute to asymptomatic giardiasis [21]. The parasite adaptations promoting cyst survival in the external environment and trophozoite infectiveness and persistence in the mammalian small intestine each contribute to being key virulence properties for this parasite to cause symptomatic disease [29]. In this work eight common symptoms recorded in human were diarrhea 75%; foul smelling greasy stool 31.8%; bloating 22%; abdominal crump 85%; anorexia 6.4%; fever 25%; vomiting 9% and constipation 16%. These were agreeing with the most important clinical symptoms are diarrhea and mal-absorption [2]. Other mention that intestinal troubles followed by nausea and anorexia, other signs could be low-degree fever, flatulence and abdominal distension with cramps occurred in acute stage, later symptoms include profuse, watery and foul-smelling diarrhea [22]. During the chronic stage lethargy, headache and muscle pain with progressive weight loss, loss of appetite and mal-absorption could be present [22]. Impaired fat absorption and staetorrhea are common in symptomatic giardiasis, stools are usually greasy and malodorous and float in water [20]. Typically, the symptoms accompanying infection include diarrhea, flatulence, upper intestinal cramps, abdominal distension, nausea, weight loss and mal-absorption [30].
Host factors such as immune status, nutritional status and age, as well as differences in virulence and pathogenicity of G. duodenalis isolates are recognized as important determinants for the severity of infection [9,12]. The colonization of trophozoites in the small intestine results in a reduction in the height of the microvilli and therefore a loss of absorptive surface area [9]. This loss of absorptive surface leads to mal-absorption of glucose, electrolytes and water, and reduces disaccharidases activity [13]. This results in the small intestine filling with mucous and fluid, and ultimately mal-digestion and hypermotility, all responsible for the clinical manifestation of diarrhea [14]. As a result, enterocytic brush border is damaged, the increased epithelial permeability leads to an inflammatory response, digestive and absorptive changes, that correlate with the brush border injury and disaccharidases deficiencies [15].