Year : 2012 | Volume
: 2 | Issue : 1 | Page : 13--19
Emerging protozoal pathogens in India: How prepared are we to face the threat?
Subhash Chandra Parija, Sidhartha Giri
Department of Microbiology, Jawaharlal Nehru Institute of Post Graduate Medical Education and Research, Puducherry, India
Subhash Chandra Parija
Department of Microbiology, Jawaharlal Nehru Institute of Post Graduate Medical Education and Research, Puducherry - 605 006
Emerging protozoal pathogens have become a major threat to human health. The number of protozoal pathogens causing human disease has been on the rise since the last two to three decades. Significant increase in the number of immunocompromised people, increase in international travel, deforestation, and widespread urban dwellings are some of the factors contributing to this changing epidemiology of protozoal diseases. Apart from Naegleria and Acanthamoeba, other free-living amoebae like Balamuthia and Sappinia are being reported to cause meningoencephalitis in humans. Plasmodium knowlesi, a zoonotic malarial parasite, has become a major cause of human malaria in Southeast Asia. Trypanosoma evansi and Trypanosoma lewisi, which normally infect horses and rodents respectively, have been reported to cause human trypanosomiasis in India. Balantidium coli is emerging as an important cause of dysentery especially in the immunocompromised population. In India, where a significant proportion of population lives in close proximity to cattle and pigs, B. coli can emerge as a significant pathogen in cases of dysentery, especially in the immunocompromised population. Babesia microti has become an important cause of transfusion transmitted babesiosis (TTB) in countries like the United States. As Babesia can be misdiagnosed as Plasmodium and blood transfusion is becoming common in India, it is necessary to develop diagnostic tests to rule out this pathogen in blood donors. Increased awareness among clinicians, pathologists, and microbiologists along with other factors like constant surveillance, improved diagnostic tests, and a high index of suspicion are important to detect and properly treat such emerging protozoal pathogens in humans.
|How to cite this article:|
Parija SC, Giri S. Emerging protozoal pathogens in India: How prepared are we to face the threat?.Trop Parasitol 2012;2:13-19
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Parija SC, Giri S. Emerging protozoal pathogens in India: How prepared are we to face the threat?. Trop Parasitol [serial online] 2012 [cited 2020 Sep 25 ];2:13-19
Available from: http://www.tropicalparasitology.org/text.asp?2012/2/1/13/97233
Parasitic infections have been known to man since ages. The number of protozoan and helminthic parasites causing human infections has increased considerably over time. Presently, there are about 300 helminthic worms and 70 protozoan pathogens known to cause disease in humans. Out of these, many are rare and accidental parasites, but about 90 species of parasites commonly cause infection in humans. 
Protozoal infections continue to cause significant morbidity and mortality throughout the world. The significant increase in the number of immunocompromised patients worldwide during the last few decades have led to the emergence of new protozoal pathogens as well as appearance of well established protozoal parasites in previously unaffected areas. The number of immunosuppressed patients is increasing every year as the human immunodeficiency virus (HIV) pandemic continues to spread in many parts of the world. What is adding to the problem is the fact that most of the new HIV infections are occurring in the developing and underdeveloped regions of the world where access to therapy is limited and so the patients gradually progress to profound immunosuppression (i.e. acquired immuno-deficiency syndrome or AIDS). In contrast, in the developed parts of the world, a majority of the immunosuppressed population are due to an increase in long-term immunosuppressive therapies for various immune-mediated disorders or malignancies, prolonged antibiotic therapy, etc. 
Apart from the increase in the number of immunocompromised patients, other factors which have contributed to the increasing burden of protozoal diseases include a rapid increase in international travel, deforestation, increase in urban dwellings, improvement in diagnostic capabilities, etc. The last few decades have seen an enormous increase in international travel which has led to transport of various protozoal parasites between continents, thus breaking the geographical barriers which used to confine several protozoal diseases to certain endemic regions. Widespread deforestation and the rapid increase in urban dwellings have led to an increase in the number of parasitic diseases caused by zoonotic protozoa. Improvements in diagnostic capabilities especially molecular methods like polymerase chain reaction (PCR) has resulted in increased sensitivity and specificity in the detection of protozoal infections.
Pathogenic and free-living amoebae like Naegleria, Acanthamoeba, and Balamuthia are found worldwide and can cause infections in humans as well as animals. All three species are known to cause infections of the central nervous system (CNS).  Out of about 30 known species of Naegleria, only one (Naegleria fowleri) is known to cause acute meningoencephalitis in humans. Various Acanthamoeba species (Acanthamoeba culbertsoni, Acanthamoeba castellanii, Acanthamoeba hatchetti, Acanthamoeba healyi, Acanthamoeba polyphaga, Acanthamoeba astronyxis and Acanthamoeba divionensis) and one species of Balamuthia (Balamuthia mandrillaris) are known to cause granulomatous amoebic encephalitis (GAE) in humans. Acanthamoeba and Balamuthia are also known to cause infections of the lung and skin. Another free-living amoeba, Sappinia diploidea, has been reported to cause encephalitis in an immunocompetent male. This is the only report available in which Sappinia has been implicated as a human pathogen.
B. mandrillaris was first isolated in 1986 from the brain of a pregnant mandrill baboon. The first human case was documented in 1991. It is the only known species belonging to genus Balamuthia which can cause GAE in humans and animals. It is similar to the GAE caused by Acanthamoeba. Balamuthiasis occurs in immunocompromised hosts like HIV/AIDS patients and intravenous drug abusers. It has also been found to affect immunocompetent hosts especially young children and older individuals.  Balamuthiasis has a subacute, chronic course which may vary from 2 weeks to 2 years. B. mandrillaris also causes skin infection similar to Acanthamoeba.
B. mandrillaris, like Acanthamoeba, has only two life-cycle stages, namely trophozoite and cyst. The trophozoite is pleomorphic and varies from 12-60 μm. The trophic amoeba is usually uninucleate but can occasionally be binucleate also. The cyst is also uninucleate and possesses three layers, an outer thin and irregular ectocyst, a middle amorphous fibriller mesocyst, and a thick inner endocyst. 
The precise niche, distribution, or food source of B. mandrillaris in the environment is not known. Humans usually get the infection by contact with contaminated soil which is the major risk factor in contracting GAE or Balamuthia amoebic encephalitis (BAE). More than 100 cases of BAE have been documented worldwide.  A majority of these infections occur in warmer climates, with a significant number of cases occurring in individuals of Hispanic origin. Balamuthiasis has been reported from many countries like Peru, Argentina, Brazil, Mexico, Venezuela, United States, Japan, Thailand, etc.  The exact number of cases of balamuthiasis worldwide may never be known, which may be due to lack of awareness, poor diagnostic facilities, and poor public health systems in the less developed countries.
Various routes of entry into the CNS have been suggested. Involvement of the CNS is thought to occur through hematogenous spread from a lesion in the lungs or the skin although in most cases a primary site of infection is not identified.  Patients with BAE have presented with facial skin lesions, rhinitis, sinusitis, and otitis media. Painless skin lesions appearing as plaques (single or multiple) appear commonly on face but may occasionally occur on trunk, hand, or feet. In many reported cases, the skin lesions precede CNS involvement. The time between the appearance of skin lesions and the onset of neurologic symptoms may vary from 1 month to 2 years.
The laboratory diagnosis of B. mandrillaris is difficult because it is not easily recovered from cerebrospinal fluid (CSF). Examination of CSF reveals lymphocytic pleocytosis along with mild to severe elevation of protein levels and normal or low glucose. Brain or skin biopsies are important diagnostic procedures. It may be difficult to differentiate between Acanthamoeba and Balamuthia in tissue sections by light microscopy due to their similar morphology. Immunofluorescence analysis of tissue sections using rabbit anti-Acanthamoeba and anti-B. mandrillaris sera is useful in distinguishing between the two parasites.  PCR-based assays are highly sensitive and specific in detection of B. mandrillaris in CSF. A PCR-based assay using ribosomal RNA (rRNA) sequences has been developed for the specific diagnosis of B. mandrillaris. PCR assays using Chelex to isolate the deoxyribonucleic acid (DNA) from B. mandrillaris could detect parasites in small cell numbers. This is important in case of most clinical samples which often contain very few amoebae. 
The case fatality rate in BAE is very high (>98%).  Combination therapies consisting of pentamidine, fluconazole, flucytosine, sulfadiazine, and a macrolide antibiotic (azithromycin or clarithromycin) have been advocated for the treatment of BAE. But treatment has to start early for a favorable outcome.  In 2010, the successful treatment of a pediatric case of B. mandrillaris meningoencephalitis has been reported using this combination therapy. 
In India, there are no reports of B. mandrillaris infection in humans till date. In 2004, the first case of meningoencephalitis due to B. mandrillaris in Southeast Asia was reported from Thailand by Intalapaporn et al.  It was reported in a 23-year-old man who had a history of road traffic accident about 6 months before he developed meningoencephalitis. After the accident, the patient developed a star-shaped ulcer in his nose which did not heal. It has been postulated that the patient got infected with B. mandrillaris during the accident when he was thrown into a swamp. This leads to speculation that B. mandrillaris might be present in the environment of tropical countries of Southeast Asia like Thailand, India, etc. So, constant vigilance and increased awareness among physicians and microbiologists is very necessary to detect this pathogenic parasite. We may be misidentifying B. mandrillaris with Acanthamoeba as both produce cysts in the brain and it is difficult to isolate B. mandrillaris from the CSF. Therefore, immunofluorescence assays with specific antisera and molecular methods like PCR need to be introduced in the laboratories for proper diagnosis. The case fatality rate for BAE is very high (>98%) and so, most of the cases are diagnosed at autopsy. Cultural ethos and expense prevent autopsies in all cases of encephalitis in developing countries like India, which may also be contributing to difficulty in detection of B. mandrillaris.
Sappinia species is the latest in the list of free-living amoebae isolated from cases of encephalitis. In 2001, Gelman et al. reported the first and the only confirmed case of amoebic encephalitis caused by Sappinia species.  It was isolated from a 38-year-old white male in Texas who was admitted to the hospital with a history of loss of consciousness, vomiting, photophobia, headache, and blurring of vision. Magnetic resonance imaging (MRI) showed a solitary 2-cm mass in the posterior left temporal lobe. A biopsy was done and the excised mass on sectioning revealed necrotizing hemorrhagic inflammation containing the trophozoites of a free-living amoebae, which was morphologically different from any of the amoeba species isolated so far from human cases. The causative agent was identified morphologically as Sappinia diploidea on the basis of hematoxylin-eosin stained smears of brain tissue. The characteristic feature of the amoebae was the presence of two tightly apposed nuclei. Cysts were not seen in the brain tissue. The patient underwent surgical excision of the tumor like mass in the brain along with antibiotic therapy and recovered without any neurologic sequelae. Later, in 2009, Qvarnstrom et al. developed a real-time PCR assay for the identification of different species of Sappinia. They confirmed the isolate to be Sappinia pedata using a real-time PCR assay and not S. diploidea as was reported initially in 2001. 
Sappinia has two life-cycle stages, trophozoite and cyst. Both the trophozoite and cyst stages are binucleate. The trophozoite measures 40-80 μm, is oblong or ovoid, and is flattened with occasional wrinkles on the surface. The cytoplasm contains contractile vacuole and food vacuoles. The cyst is round and measures 15-30 μm. 
Sappinia had never before been implicated in human disease although it has been isolated from different environmental sources like soil, fresh water, forest litter etc. This unusual finding has led to speculation that other free living amoebae in the environment may be causing encephalitis and other infections in the human population. Diagnosis of infections caused by free-living amoebae is difficult due to various reasons. These infections are so uncommon that most clinicians and microbiologists are not familiar with the clinical symptoms and the methods of isolation of these pathogens from clinical specimens. There are only few diagnostic laboratories which are capable of identifying these parasites to the species level.
Other than the four Plasmodium species causing malaria (Plasmodium falciparum, Plasmodium vivax, Plasmodium malariae, Plasmodium ovale), Plasmodium knowlesi has been found to cause natural infection in humans. Natural infection with P. knowlesi vary according to geographic locations (highest prevalence in Malaysian Borneo), but cases have been increasingly detected in other Southeast-Asian countries also (Thailand, Vietnam, Cambodia). ,,
P. knowlesi was first isolated by Robert Knowles and B.M Das Gupta, who were able to transmit the monkey malaria to humans in 1932. P. knowlesi was used as a pyretic agent in the treatment of neurosyphilis. But it was later replaced by P. vivax as many patients developed complications with P. knowlesi malaria.  More recently, it has also been used in the analysis of requirements for erythrocyte invasion and in vaccine studies.
P. knowlesi circulates among the long tailed macaques (Macaca fascicularis) and pig tailed macaques (Macaca nemestrina), which are found in the jungles of Southeast Asia. The natural vectors of P. knowlesi belong to the Anopheles leucosphyrus group. These mosquitoes are attracted equally to humans and monkeys and feed predominantly in the forest and in the forest fringe after dusk. The fact that the vector mosquitoes prefer forest areas for feeding probably explains why there has been no full blown epidemic of P. knowlesi malaria till now.
Microscopy based detection of P. knowlesi has failed because the early trophozoite forms of the parasite resembles P. falciparum, whereas the late trophozoite forms are similar to that of P. malariae. Early trophozoites appear as ring forms and occasionally, multiple ring forms and double chromatin dots are seen in each erythrocyte, similar to P. falciparum. The late trophozoite forms show "band forms" similar to P. malariae.  To date, the most effective test to confirm the diagnosis of P. knowlesi infection is by PCR specific for multicopy genes, such as small subunit rRNA and mitochondrial cytochrome b. 
The first natural infection with P. knowlesi was documented in 1965 in a man who returned to USA after a visit to peninsular Malaysia.  There was another report in 1971 of P. knowlesi malaria in a man in peninsular Malaysia.  After that, no natural infection with P. knowlesi was reported worldwide till 2004 when Singh et al., reported a high prevalence of natural infection by P. knowlesi in humans.  All these cases were misdiagnosed as P. malariae by microscopy but were found to be P. knowlesi by a PCR assay. Janet Cox-Singh et al., in 2008, found P. knowlesi malaria to be potentially life threatening and described four fatal cases of P. knowlesi malaria.  All the four PCR confirmed cases of P. knowlesi malaria presented with severe abdominal pain along with a history of fever and chills. There was also marked hepatorenal dysfunction which is a feature of severe falciparum malaria. The 24 hour asexual life cycle of P. knowlesi is the shortest of all known Plasmodium species, which leads to daily schizont rupture and attendant fever spikes. Due to massive parasitemia in such cases, even a short delay in proper diagnosis and treatment could increase the risk of complications.
In contrast, P. malariae causes a low parasitemia and a less proportion of symptomatic cases. Because P. knowlesi could be easily misdiagnosed as P. malariae by microscopy and PCR assays are not commonly available, it has been recommended that any symptomatic malaria with hyperparasitemia and parasite morphology resembling that of P. malariae be diagnosed as P. knowlesi in Malaysia and some other Southeast Asian countries (Thailand, Cambodia, Vietnam etc.) which are inhabited by the nonhuman primate hosts. 
Till date, there have been no reports of P. knowlesi malaria from India. But we have the vectors (Anopheles dirus)  and the primate hosts (pigtailed macaques) in the Northeastern part of India. As P. knowlesi can be easily misdiagnosed as P. malariae or P. falciparum by light microscopy, we might be missing cases of P. knowlesi malaria in India. Therefore, it is necessary to supplement light microscopy with other advanced diagnostic tests like PCR which will definitely help us to detect cases of P. knowlesi. Apart from improved diagnostic facilities, constant surveillance along with an increased awareness among physicians and microbiologists is necessary to detect any new infection due to P. knowlesi in India.
Human trypanosomiasis is endemic in Africa and South America. Trypanosomes are flagellated protozoan parasites. Human African trypanosomiasis (HAT) or sleeping sickness is caused by Trypanosoma brucei gambiense (west and central Africa) and Trypanosoma brucei rhodesiense (East Africa), both of which are morphologically identical subspecies of Trypanosoma brucei. South American trypanosomiasis or Chagas' disease is caused by Trypanosoma cruzi.  Trypanosoma rangeli is a non-pathogenic trypanosome found in the blood of humans in Venezuela and Colombia. Apart from these trypanosomes, there are others which are known to infect animals. Trypanosoma evansi causes "surra" in horses and mules, Trypanosoma equinum causes "mal de caderas" in horses in South America, Trypanosoma brucei brucei (animal strain) causes "Nagana" in cattle, Trypanosoma lewisi infects rats, etc.
In the last few years, there have been reports of zoonotic trypanosomes infecting humans from countries like India and Thailand. , This is very important from public health point of view because these zoonotic trypanosomes are found in many parts of the world.
Till date, four cases of trypanosomiasis in humans have been reported from India. Two cases of self-limiting febrile illness due to T. lewisi were reported in 1974.  The couple lived in a rat infested village area and the symptoms resolved without any specific treatment after two to three days. In 2005, Joshi et al., reported the first human infection caused by T. evansi, which is known to cause an animal trypanosomiasis known as "surra".  Blood smear stained with Giemsa from an Indian farmer who had a fluctuating trypanosome parasitemia along with febrile episodes for 5 months showed large number of parasites with morphology typical of T. evansi. The parasites were monomorphic, slender, flagellated, dividing trypomastigote-form trypanosomes. The card agglutination test for trypanosomiasis (CATT)/T. evansi, obtained from the Institute of Tropical Medicine in Belgium, was done which was strongly positive with whole blood and serum diluted up to 1:64. PCR amplification of the internal transcribed spacer (ITS) of trypanosome-specific ribosomal DNA using primers ITS1/2 further confirmed the parasitologic and immunologic diagnosis of T. evansi infection. Analysis of CSF indicated no invasion of the CNS by the trypanosome. The patient was treated with suramin, a drug extensively used for the treatment of human African trypanosomiasis. The patient greatly improved with no other side effects during and after treatment. The route of infection was not known. However, a scar on one of the fingers of the patient was noted during initial admission which led to the speculation that contact with infected animal blood which is an occupational hazard associated with cattle farming may have been the portal of entry for the pathogen.
Another case of human trypanosomiasis in India, caused by zoonotic trypanosomes, was reported by Kaur et al., in 2007.  They reported a case of trypanosomiasis caused by the rodent parasite T. lewisi in a 2-month-old infant in urban Mumbai. Similar case reports have emerged from other countries like Thailand. In 2007, Sarataphan et al. reported a T. lewisi-like (Herpetosoma) infection in a sick infant from Thailand.  Trypanosomes were observed in the peripheral blood of a 45 day old infant who presented with fever, anemia, cough and anorexia. Morphologically, the trypanosomes were similar to T. evansi and statistically different from T. lewisi-like parasites isolated from a naturally infected indigenous rat. But, duplicate PCR assays flanking trypanosome rRNA ITS1 resulted in amplicons that matched with the expected size of T. lewisi-like parasites. So, based on molecular results, it was concluded that the Thai infant was infected with T. lewisi-like (Herpetosoma) species. These trypanosomes utilize fleas and rodents as natural hosts, which was corroborated by the identification of Ctenocephalides felis fleas in the infant's dwellings. 
Trypanosomiasis is endemic in animals in India. Trypanosomes are found in a wide variety of animals including horses, camels, donkeys, dogs etc.  Therefore, although sporadic cases of trypanosomiasis caused by zoonotic trypanosomes have been reported in India, we may not be detecting all cases due to lack of proper diagnostic facilities as well as clinicians being unaware of such infections in this part of the world. It is necessary to develop diagnostic facilities with skilled microbiologists and technicians capable of diagnosing such cases. It is also equally important to create awareness among physicians about such emerging zoonotic trypanosomiasis because early diagnosis and proper treatment is necessary for a favorable outcome.
Balantidium coli is the only ciliate protozoan which is known to infect humans. Balantidiosis is a zoonotic disease and is acquired by humans through the feco-oral route from the natural hosts, the pigs, where it is asymptomatic. Contaminated water with pig or human feces is the most common source of infection. Human-human transmission can also occur. Humans may remain asymptomatic or may suffer from symptoms similar to amoebic dysentery. Death is uncommon in balantidiosis but it can cause chronic debilitation.
B. coli has been found as a pathogen in immunocom-promised population especially in AIDS cases and in malignancies.  A 71-year-old Greek woman suffering from anal cancer, fever, and intermittent diarrhea was found to have B. coli in her lungs when a wet mount was examined from her bronchial secretions. Despite treatment with metronidazole (drug of choice for balantidiosis), the patient expired due to cardiac arrest although the exact cause of her death was not ascertained.  In another case, a 54-year-old French butcher with acute diarrhea suffered colonic perforation but recovered after doxycycline treatment and colectomy. B. coli was found in his stool.  Similar cases of diarrhea due to B. coli have also been reported from patients with malignancies.  With the rapid increase in the number of immunocompromised patients worldwide, B. coli can emerge as an important pathogen in this patient population.
Only one case of human infection with B. coli has been reported from India. In 2007, Umesh from India reported B. coli to be present in the urine of a 29-year-old woman in Mumbai. He postulated that B. coli trophozoites are highly pathogenic and can metastasize from the gastrointestinal tract to other parts of the body through the blood stream.  But, further diagnostic tests like stool examination is necessary to confirm such hypothesis. B. coli has been reported in animals like pigs, cattle, etc. from different parts of India. The first report of severe cattle diarrhea due to B. coli was reported from India by Randhawa et al., in 2010.  In another study by Bauri et al., a high prevalence of B. coli infection (93%) was found in pigs in Jharkhand, India.  In India, a significant proportion of the population lives in close proximity to animals like pigs and cattle. The number of immunocompromised individuals in India is on the rise because of the HIV pandemic and rapid increase in different types of malignancies. There has also been an increase in life expectancy leading to more number of older people who are immunocompromised and have other chronic medical conditions. Therefore, it is necessary to have a high index of suspicion in all cases of dysentery especially in the immunocompromised population to detect this pathogen.
Babesia species cause babesiosis in animals and humans. These are intraerythrocytic protozoan parasites transmitted to hosts primarily by tick vectors. Human infection is caused by three species: Babesia bovis, Babesia divergens (cattle strain), and Babesia microti (rodent strain). Recently, a few new strains of Babesia have been identified in humans (WA1, CA1, KO1). , Human infection with Babesia spp may cause mild malaria-like fever. It can also cause severe disease in splenectomized patients and HIV-positive cases.
Although the first case of human babesiosis was reported way back in 1957, Babesia spp have recently emerged as a public health concern for humans, primarily in the United States. Human cases of babesiosis have been reported from various parts of the United States like Connecticut, Massachusetts, New York, and Rhode Island.  With the emergence of babesiosis as an emerging public health problem in the United States, concern for blood transfusion safety has grown, because of the intraerythrocytic location of the parasite. Although sporadic cases of transfusion transmitted babesiosis (TTB) have been reported since the 1980s, the number of cases has increased steadily over the last 30 years. Eight deaths have been attributed to TTB in the United States since November 2005.  This increase in the number of deaths due to TTB was concomitant with an increase in incidence of TTB, rising from 42 reports in the 8-year period from 1997 to 2004 to over 50 reports in the 3-year period from 2005 to 2007.  Despite the current recognition that there has been a steady rise in TTB over the years, the options available to prevent the infection due to transfusion are limited. So, TTB warrants our attention and action without further delay.
Few cases of babesiosis have been reported recently from Asian countries including India and Korea. In India, the first case of human babesiosis was reported by Marathe et al., from Baroda (Gujarat) in 2005.  A 51-year-old male patient who came to Baroda from Gwalior (Madhya Pradesh) presented with fever, anorexia, and vomiting. Peripheral blood smear stained with Leishman's stain showed ring forms within erythrocytes which were initially confused with Plasmodium species (especially P. falciparum) and the patient was started on anti-malarial drugs to which he did not respond. Later, a careful examination of the smears revealed typical pairs and tetrads of pear-shaped trophozoites, schizont forms devoid of hemozoin pigment, extracellular merozoites, and intraerythrocytic multiple merozoites. So, the parasite was identified as Babesia species. To rule out co-infection with Plasmodium species, tests were done to detect histidine-rich protein II (HRPII) and other Plasmodium antigens, all of which were found to be negative. The patient was treated with clindamycin and became afebrile after 2 days. Another case of human babesiosis was reported from Korea by Kim et al., in 2006, which was caused by a novel type of Babesia species (KO1), similar to ovine Babesia. 
Malaria is endemic in many parts of India. Peripheral smears of babesiosis can be easily confused with Plasmodium species. So, careful examination of peripheral smears and surveillance studies may be necessary to know the actual prevalence of human babesiosis in India. Along with human babesiosis, TTB has to be kept in mind in a country like India where blood transfusion is done on a large scale. It is very necessary to develop proper screening methods for babesiosis in donors as is present for other pathogens (HIV, Hepatitis B virus, Hepatitis C virus, malaria).
Recently, in 2012, Yuan et al., from China, reported a case of a Babesia spp-like relapsing infection in a woman caused by a newly described microorganism related to the Apicomplexa. The new organism has been identified as Colpodella spp-like parasite and this is the first reported human infection caused by this parasite worldwide although further studies are still required to describe this organism and confirm these findings in humans. 
Protozoal pathogens are emerging as causes of human disease in many parts of the world including India. The number of newly identified protozoal pathogens causing human infections is on the rise. Previously identified protozoal pathogens which caused sporadic cases of infections in humans are now known to cause more frequent disease leading to a rise in morbidity and mortality caused by them. An increase in awareness among clinicians and microbiologists about such emerging pathogens is vital for early diagnosis and proper treatment. Constant surveillance, a high index of suspicion, and improvement in diagnostic methods are other factors essential for the detection of these emerging protozoal diseases.
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