Giardiasis

Giardiasis is a water borne parasitic infection caused by protozoa, Giardia duodenalis. It is the third most common cause of diarrhea after Rota virus and Cryptosporidium app. The chronicity of diarrhea caused by G. duodenalis is more common than of cryptosporidium spp even in the immunocompetent hosts. However, most of cases of giardiasis is asymptomatic (around 69%). They are widely distributed worldwide and more prevalent in the countries with poor sanitation and bad food hygiene practices especially in the developing and under developed countries.

Life cycle:

There are two distinct forms of the protozoa, trophozoites and cysts form.

1.       Trophozoites are motile form and show the falling leaf like motility. They possess four pairs of flagella measuring about 12-15 and 5-15 micrometer in diameter. It contains two nuclei and with the help of flagella it attaches to intestinal mucosa by sucking discs. They multiply by longitudincal binary fission. No Sexual reproduction has been reported yet in the giardia.

2.       Cyst form of Giardia is infective form with thick wall. The cyst form contains four nuclei and size ranges from 8-14 micrometer. A cyst divides to give two trophozoites.

Human get infected with ingested of contaminated water with infective cyst forms. Once this cyst forms crosses the acid barrier of stomach, they start excyst in small intestine to form two trophozoites. They favor alkaline pH of duodenum and jejunum. The attach to the small intestine microvilli via the sucking discs and move freely to the lumen actually to the soft mucosa and submucosa. Unlike the cyrtosporidium they don’t invade the tissue and just attach on microvilli and damage it causing malabsorption and diarrhea.

Sometimes trophozoites can also be seen in the stool but they can’t tolerate the extreme environmental condition outside, however cysts can resist and hence use for diagnosis.

Trophozoites multiply by longitudinal binary fission, remaining in the lumen of the proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk. Encystation occurs as the parasites transit toward the colon. The cyst is the stage found most commonly in non-diarrheal feces. Because the cysts are infectious when passed in the stool or shortly afterward, person-to-person transmission is possible. While animals are infected with Giardia, their importance as a reservoir is unclear.

Classification:

Altogether there are 9 assemblages of Giardia spp. named as A, B,C, D, E, F, G and H.  The assemblages A and B are only found to infect the humans, medically important species.

Assemblage A. Zoonotic and anthroponotic transmission (primates, dogs, cats) and reported from diarrheal stool samples of India, Spain and Turkey.

Assemblage B. It is also transmitted by zoonotic and anthroponotic routes but only reported in Malaysia, Netherland and Ethiopia.

Pathogenesis:

The major virulence’s factors of Giardia spp are flagella and antigenic variations, variant-specific surface proteins (VSPs) among the species. A dense coat of VSPs covers the surface of Giardia trophozoites, and a single VSP is normally dominating in a population of parasites, which is used by the protozoa to escape the immune response of the host.   The antigenic variation also induces immune response of host and the damage is due to host inflammatory response to giardia. The protozoa can also damage the microvilli and lead to malabsorption.

The mechanism of pathogenesis for Giardia is non invasive one unlike that of Crytosporidium spp. The protozoa don’t penetrate the cells and their pathogenesis is not clearly understood. Even 10 Giardia cysts can cause the infection to human.

After excystation, the motile trophozoites are released into the small intestine. The trophozoites then adhere to the epithelial cells via a specialize ventral suck device. The protozoa and host cells attachment target specific signaling networks including those of caspases. The caspases then activate the apoptosis mechanism leads to death/loss of intercellular junctions. The reduced expression and relocation of tight junctions such as Zo1, caudin-1, F-actin and alpha actinin result in increased intestinal permeability and decreased transepithelial resistance. The disruption also leads to cytoskeleton rearrangement and barrier dysfunction. These mechanisms contribute to pathophysiological features such as paracellular leakages-electrolyte secretion, malabsorption and finally to exudative diarrhea. The tight junction alterations are associated to secretory diarrhea due to an increase in chloride ion concentration and loss of absorptive functions. The pathological observations on symptomatic has characteristic features of villous shortening, microvilli atrophy and increase cell death and destruction of the epithelial barriers. Consequently, enhanced fluid secretions from the crypts cells is observed.

Clinical manifestations:

Commonly the clinical symptoms manifest in 7-10 days and last for 1-3 weeks.  Most of symptomatic giardiasis have common symptoms like severe diarrhea, abdominal cramps, bloating, flatulence, nausea and vomiting.

The chronic giardiasis in immunocompromised individuals may have increases gas, dehydration, burping, loose stools and slowed growth which may last for 2 months to years.

In both of the cases, weight loss and dehydration are frequent.

Immune response by the host

Infection with Giardia is not often accompanied by inflammation. The protozoa is poor cytokine inducer. Higher prevalence of symptomatic Giardiasis is observed in infants and self-limiting diarrhea is common in toddlers to endemic areas. Rarely symptomatic infection occurs after pre-exposure. This shows the role of sIgA antibody to prevent the infections. The neutralizing antibodies are the protective immune response for Giardiasis. However, severe giardiasis mostly occurs in underweight children with pre-existing malnutrition.

Laboratory Diagnosis

·         Light Microscopy: Iodine/Giemsa

·         Immunochromatography

·         Flow cytometry / ELISA

·         Molecular tools convention and real time PCR

Prevention

·         Good hygiene practice

·         Safe drinking water

·         Hand washing

·         Safe travelling