Epidemiology

1. Geographical distribution and risk groups:

Microsporidiosis in humans occurs world-wide, but prevalence data vary widely because of the unreliability of detection methods (Bryan and Schwartz, 1999).

Since 1985, microsporidia have been identified as a cause of opportunistic infections associated with persistent diarrhoea and weight loss in persons with AIDS (Weber et al., 2000).

The risk groups included travelers (Wichro et al., 2005), malnourished children (Mungthin et al., 2001), organ transplant recipients (Mohindra et al., 2002 and Lanternier  et al. 2009), contact lens wearers (Lewis et al., 2003), and the elderly (Lores et al., 2002).

Recently, intestinal microsporidiosis have been detected widely among immunocompetent patients. Mungthin et al. (2001) in Thailand detected microsporidial spores in 5.9 % immunocompetent children and 4% immunocompetent child-care workers. Also, Nkinin et al. (2007) in Cameron identified microsporidia spores in 67.5% of immunocompetent patients

In USA, Dascomb et al. (2000) detected intestinal microsporidiosis in 4.1% of examined cases. Also, Carlson et al. (2004) reported the first case of microsporidiosis (Encephalitozoon species) in a pancreas/kidney transplant recipient.

In Europe, microspordiosis was detected in Switzerland (Katzwinkel-Wladarsch et al. 1997) , Austria(Wichro et al. 2005),  Portugal (Matos et al. 2002 and Lobo et al. 2008  )and France( Raynaud et al. ,1998 and  Cotte et al. ,1999).

In Germany, Ullrich  et al. (1991) detected E. bieneusi in 4.3% of examined patients, Dengjel et al. (2001) detected microsporidia in  7.7% of examined patients and  Muller et al. (2001) found microsporidia in 6% of  travelers.

In Spain, Lores et al. (2002) detected intestinal microsporidia in 17% of HIV-negative elderly patients with diarrhoea. Abreu-Acosta et al. (2005) recorded that 11.6% of examined cases were microsporidia positive.

In Latin America, Sulaiman et al. (2003) found that 3.9% of HIV-infected Peruvians cases were microsporidia-positive patients. Bern et al. (2005) in Peru found that 4.1% of examined patients had microsporidiosis. Velásquez et al. (2005) in Argentina detected intestinal microsporidiosis in 11.5% of examined patients. Chacin-bonilla et al. (2006) detected intestinal microsporidiosis in 17.6% of HIV-positive Venezuelans patients with diarrhoea. Also, Bedoya et al. (2008) in Colombia detected the presence of Encephalitozoon intestinalis among Colombian patients.

In Asia, microsporidiosis was detected in India (Mohandas et al. ,2002 and  Kumar et al. ,2005 ), Nepal( Shrestha and Enriquez, 2001)and Thailand (Viriyavejakul et al. 2009). In Malaysia, Norhayati et al. (2008) found that 13% of immunocompetent patients were microsporidia-positive and Lono et al. (2010) detected intestinal microsporidia in 21.2% in cases from Orang Asli community.

In Africa, microsporidiosis was detected in Cameron (Breton et al. 2007 and Nkinin et al. 2007), South Africa (Samie et al. ,2007) ,Ethiopia (Endeshaw et al., 2005 and 2006), Uganda (Tumwine et al. ,2005 and Mor et al ., 2009) and Tunisia( Chabchoub et al. ,2009).

In Egypt, Abaza et al. (1995) reported that 2.3% of immunocompromised patient were infected. In Assiut, Hamza and Abd El-Megeed (1999) detected intestinal microsporidiosis in 41% of   food handlers in Assiut university hospital

Omran et al. (2000) in Egypt identified microsporidia spores in 7% of cancer patients admitted to south Egypt cancer institute.

 Ali et al. (2000) in Egypt detected intestinal microsporidiosis in 8.3% patients suffering from chronic renal failure attending the Dialysis Unit of Zagazig University Hospital.

 El-Diffrawy et al (2002) detected intestinal microsporidia in 12% of immunocompromised patients attending Alexandria University Hospital.

El Shazly et al. (2006) in Egypt detected intestinal microsporidiosis in 3.2% of patients attending Mansoura University Hospitals' Clinics.

2. Sources of human infection and modes of transmission:

Microsporidiosis is an emerging, recently recognized infection in humans, and only a few studies have been conducted to determine the source and mode of transmission. (Deplazes et al., 2000).

The majority of microsporidian infections in mammals are believed to occur through ingestion or inhalation of spores. Vertical or transplacental transmission of microsporidiosis has not been reported to occur in humans but has been reported to occur in carnivores, including foxes and domestic dogs, and occasionally in non human primates, horses, rabbits, and rodents (Snowden et al., 1998 and Didier et al., 2000).

On rare occasions, microsporidiosis was transmitted through direct contact or trauma. Experimentally, microsporidia infections have been transmitted to laboratory animals by intraperitoneal, intravenous, intrarectal, intratracheal and intracerebral inoculations (Snowden et al., 1998).

2.1. Vertical and horizontal transmission:

Vertical transmission of microsporidiosis from mother to offspring has been described in rodents, rabbits, carnivores, and non-human primates (Snowden et al., 1998 and Snowden and Shadduck, 1999).

Vertical transmission of microsporidiosis in humans has not been reported. The presence of microsporidia in the respiratory and intestinal tracts of infected individuals and the excretion of spores in urine and feces indicate that horizontal transmission is possible through routes that include fecal–oral transmission, oral–oral transmission, inhalation of contaminated aerosols, and ingestion of contaminated food and water (Weber et al., 2000 and Deplazes et al., 2000).

Risk factors associated with microsporidiosis that support horizontal transmission included homosexual practices, intravenous drug use, and exposure to water in swimming pools and hot tubs or occupational contact with water (Dascomb et al., 2000 and Deplazes et al., 2000).

 Examples of horizontal transmission of microsporidia between animals further support the likelihood that the same species can be transmitted between humans. For example, naive mice housed with E. cuniculi-infected mice subsequently became infected, and conversely, culling infected animals resulted in clearance of E. cuniculi from the affected colonies (Liu et al., 1988).

2.2. Zoonotic transmission:

Many species of microsporidia found to infect humans also infect a wide range of animals supporting the likelihood that zoonotic transmission occurs. Direct evidence of zoonotic transimission from domestic animals to children has been reported (Cama et al., 2007).

E. bieneusi infections were detected in pigs (Sak et al., 2008 and Reetz et al., 2009), calves (Santin et al., 2005), goats (Cama et al., 2008), llamas (Dengjel et al., 2001).

Also, E. bieneusi infections were detected in cats (Santın et al., 2006), dogs (Santín et al., 2008), rabbits (Del Aguila et al. 1999), macaques (Pourrut et al. 2002), wild boars (Del Aguila et al. 2004), beavers, foxes, muskrats, otters, and raccoons (Abe  et al., 2009).

E. bieneusi was identified in birds, i.e., chickens (Reetz et al., 2002), ostriches, and pigeons (Haro et al. 2005) captive exotic birds (Kasicková  et al., 2009)

Thus, mammals and birds can sustain a reservoir of  microsporidian spores of species known to infect people (Slodkowicz-Kowalska et al. 2006).

Despite the long list of mammals susceptible to E. bieneusi, zoo animals have not been investigated comprehensively. However, such animals have the potential to transmit zoonotic pathogens because of their accessibility to zoo visitors and contacts with zookeepers and personnel (Lobo et al. 2003).

2.3. Water borne transmission:

Microsporidian spores are environmentally resistant and survive for extended periods of time in water. Also, the spores are relatively small and not easily trapped by filtration, and the infectious dose is probably reasonably low (Franzen and Muller, 1999b).

The transmission of microsporidia by contaminated drinking water has been supported by studies detecting human virulent strains of microsporidia in water sources (Lee, 2008).

Many species of microsporidia that infect humans have been identified in various water sources including ground, surface and ditch water. In epidemiologic studies, risk factors associated with human microsporidiosis included exposure to hot tubs, occupational water, and drinking water (Didier et al., 2004 and Graczyk et al., 2007).

In a study reported by Lobo et al. (2008), microsporidia (E. bieneusi), Cryptosporidium, and Giardia were detected in raw surface water, groundwater, treated water, and processed water sites in Portugal. The E. bieneusi isolates in these water samples were of human and animal genotypes.

In Spain, microsporidia were identified among 2 of 8 water samples from drinking water treatment plants, 5 of 8 water samples from wastewater treatment plants, and one of 7 river water samples tested by Izquierdo et al. (2008).

A preliminary report suggested swimming in rivers, ponds and lakes was associated with intestinal microsporidiosis in HIV patients (Watson et al., 1996).

Dowd et al. (1998) identified E. intestinalis in surface water and groundwater and E. bieneusi was identified in surface water in the United States.

Cotte et al. (1999) in France detected waterborne outbreak in 200 persons due to tap water occurred in the 1995 summer, without evidence of fecal contamination of water.

Arcay (2000) has identified microsporidia in an array of river and lake waters in Venezuela.

Fournier et al. (2000) identified the presence of E. bieneusi from the River Seine in France from 25 samples taken over a one-year-period.

Hutin et al. (1998) conducted a case-control study with HIV-infected patients who showed that the only two factors associated with the intestinal microsporidiosis were swimming in a pool and homosexuality. This suggests that transmission is via the faecal–oral route and possibly through contaminated water.

Microsporidia are of concern in recreational water as the spores of some varieties (e.g. E. cuniculi) can contaminate the environment via urine as well as faeces (Slifko et al., 2000).

Dowd et al. (1998) have confirmed the presence of E. intestinalis and Vittaforma cornea in tertiary sewage effluent surface water suggesting that microsporidia can survive the wastewater process, including mixed medium filtration and chlorination.

Fournier et al. (2002) conducted a one-year-study of microsporidia occurrence in six different swimming pools in Paris, France .Two were pools used by babies, two used by children, one used by adults and one hot tub used by homosexual men in a private club. Of the 48 samples analysed, one proved positive for microsporidia (from one of the children’s pool), one for Cryptosporidia and none for Giardia. The positive detection of microsporidia was thought to be that of Endoreticulatus shubergi, a microsporidia usually found in invertebrates suggesting insect contamination of the pool. The good quality of the pool water reflects on the following procedures:

v The sourcing of pool water from public supply which is already disinfected.

v The pools’ utilisation of a combination of filtration and disinfection system using chlorine, bromide or ozone.

The study concluded that swimming pools are rarely contaminated with microsporidia and the risk of contamination through swimming pools is limited.

2.4. Food borne transmission:

Microsporidia are among the parasites of concern for food-borne transmission as a result of globalization of food, faster transport of food, increasing travel of consumers, and changes in food consumption patterns (Slifko et al., 2000 and Orlandi et al., 2002).

Buckholt et al. (2002) identified E. bieneusi in swine at a slaughterhouse in Massachusetts, U.S.A. Also, Thurston-Enriquez et al. (2002) discovered that DNA from human pathogenic microsporidia was present in all water sources examined. Microsporidia in irrigation water could adhere to the surface of fruits and vegetables. Since spores are extremely resistant to damage, they may remain viable on the produce for weeks or months. These facts also suggest that microsporidia may be present in juice products.

The potential for transmission by contaminated food sources has been supported by studies detecting human virulent strains of microsporidia in slaughter house animals and dairy from cows (Dowd et al., 2003 and Lee, 2008).   

In Egypt, Diab et al (2010) detected Microsporidia in the intestine of commonly consumed fish in Alexandria and suggested that these parasites can have great impact on the human health.