Symptoms caused in humans 1731 Giardiasis

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Giardiasis is self-limiting in most people. The short-lived acute phase is characterised by flatulence with sometimes sulphurous belching and abdominal distension with cramps. Diarrhoea is initially frequent and watery but later becomes bulky, sometimes frothy, greasy and offensive. Stools may float on water. Blood and mucus are usually absent and pus cells are not a feature on microscopy. In chronic giardiasis, malaise, weight loss and other features of malabsorption may become prominent. Stools are usually pale or yellow and are frequent and of small volume and, occasionally, episodes of constipation intervene with nausea and diarrhoea precipitated by the ingestion of food. Malabsorption of vitamins A and Bj2 and D-xylose can occur. Disaccharidase deficiencies (most commonly lactase) are frequently detected in chronic cases. In young children, 'failure to thrive' is frequently due to giardiasis, and all infants being investigated for causes of malabsorption should have a diagnosis of giardiasis excluded (Smith et al., 1995a; Girdwood and Smith, 1999a).

Cyst excretion can approach 107/g faeces (Danciger and Lopez, 1975). The prepatent period (time from infection to the initial detection of parasites in stools) is on average 9.1 days (Rendtorff, 1979). The incubation period is usually 1-2 weeks. As the prepatent period can exceed the incubation period, initially a patient can have symptoms in the absence of cysts in the faeces.

17.3.2 Cryptosporidiosis

In immunocompetent patients

Cryptosporidium is a common cause of acute self-limiting gastroenteritis, symptoms commencing on average 3-14 days post-infection. Symptoms include a 'flulike illness, diarrhoea, malaise, abdominal pain, anorexia, nausea, flatulence, malabsorption, vomiting, mild fever and weight loss (Fayer and Ungar, 1986). From 2 to more than 20 bowel motions a day have been noted, with stools being described as watery, light-coloured, malodorous and containing mucus (Case-more, 1987). Severe, cramping (colicky) abdominal pain is experienced by about two-thirds of patients and vomiting, anorexia, abdominal distension, flatulence and significant weight loss occur in fewer than 50% of patients. Gastrointestinal symptoms usually last about 7-14 days, unusually 5-6 weeks, while persistent weakness, lethargy, mild abdominal pain and bowel looseness may persist for a month (Casemore, 1987). In young malnourished children, symptoms may be severe enough to cause dehydration, malabsorption and even death. Histopathol-ogy of infected intestinal tissue reveals loss of villus height, villus oedema and an inflammatory reaction. Mechanisms of severe diarrhoea are primarily consequences of malabsorption, possibly due to a reduction of lactase activity. The ratio of symptomatic to asymptomatic cases is not known.

Illness and oocyst excretion patterns may vary owing to factors such as immune status, infective dose, host age and possible variations in the virulence of the organism; however, oocyst shedding can be intermittent and can continue for up to 50 days after the cessation of symptoms (mean: 7 days). In humans, the prepatent period is between 7 and 28 days. The mean incubation period (time from infection to the manifestation of symptoms) is 7.2 days (range 1-12) with a mean duration of illness of 12.2 days (range 2-26) (Jokipii and Jokipii, 1986). As the prepatent period can exceed the incubation period, initially a patient can have symptoms in the absence of oocysts in the faeces.

Oocyst excretion by either human or non-human hosts can be up to 107/g during the acute phase of infection. Infected calves and lambs excrete up to 109 oocysts daily for up to 14 days (Blewett, 1989).

In immunocompromised patients

In patients with Acquired Immune Deficiency Syndrome (AIDS), other acquired abnormalities of T lymphocytes, congenital hypogammaglobulinemia, severe combined immunodeficiency syndrome, those receiving immunosuppressive drugs and those with severe malnutrition, symptoms include very frequent episodes of watery diarrhoea (between 6 and 25 bowel motions daily, passing between 1 and 20 litres of stool daily). Associated symptoms include cramping, upper abdominal pain, often associated with meals, profound weight loss, weakness, malaise, anorexia and low-grade fever (Whiteside et al., 1984). Infection can involve the pharynx, oesophagus, stomach, duodenum, jejunum, ileum, appendix, colon, rectum, gall bladder, bile duct, pancreatic duct and the bronchial tree (Soave and Armstrong, 1986; Cook, 1987). Except in those individuals in whom suppression of the immune system can be relieved by discontinuing immunosuppressive therapies, symptoms can persist unabated until the patient dies (Soave and Armstrong, 1986). Cryptosporidiosis in the immunocompro-mised can be a common and life-threatening condition in developing countries, causing profuse intractable diarrhoea with severe dehydration, malabsorption and wasting. AIDS triple therapies can reduce the severity of the clinical consequences of cryptosporidiosis. Oocyst excretion can continue for 2-3 weeks after the disappearance of symptoms (Soave and Armstrong, 1986).

17.3.3 Cyclosporiasis

Cyclosporiasis is a 'flu-like illness, and diarrhoea with weight loss, low-grade fever, fatigue, anorexia, nausea, vomiting, dyspepsia, abdominal pain and bloating have been described as symptoms (Ortega et al., 1993; Huang et al., 1995; Fleming et al., 1998). The incubation period is between 2 and 11 days (Soave, 1996) with moderate numbers of unsporulated oocysts being excreted for up to 60 days or more. In immunocompetent individuals the symptoms are self-limiting and oocyst excretion is associated with clinical illness, whereas in immunocompromised individuals diarrhoea may be prolonged. The self-limiting watery diarrhoea can be explosive, but leukocytes and erythrocytes are usually absent. Often, diarrhoea can last longer than 6 weeks in immunocompetent individuals. The diarrhoeal syndrome may be characterised by remittent periods of constipation or normal bowel movements (Ortega et al., 1993). Malabsorption with abnormal D-xylose levels has also been reported (Connor et al., 1993).

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