EMERGING ILNESSESGROUP - IV PRESENTATION

ENCEPHALITOZOON HELLEM

Microsporidia, such as E. hellem, naturally infect birds. From a study of 570 birds from environments ranging from captive to free-range, 20 of those birds were found to shed Encephalitozoon hellemspores. Often species of parrots are the most infected. Of the eleven species that carried these spores, eight of them were aquatic birds. It is plausible then that E. hellem may originate not only from livestock birds as previously studied, but also from aquatic birds. Of these aquatic birds, E. hellem is most prevalent in birds who come into frequent contact with surface water indicating the microbes' ability to survive in water, and even longer in waters at lower temperatures. Studies have shown that a single waterfowl can introduce into the water approximately 910,000,000 microsporidia spores that infect humans, majority of which are E. hellem. This introduction is all via fecal matter where the E. hellem spores flourish until they come into contact with host cells. Encephalitozoon hellemis not known to live in any other type of environment and has thus only been found as fecal borne.

Encephalitozoon hellem was initially dectected and isolated in 1991 from three AIDS patients who were suffering from keratoconjunctivitis, among other ailments. Conjunctival scrapings and corneal tissue samples were taken from each of the three patients and were tested using SDS-PAGE analysis and Western Blotting . All three isolates had identical banding patterns and appeared similar to another species of Encephalitozoon, E. cuniculi, and the new AIDS related microsporidian was then given its name, Encephaliozoon hellem.In 1994, another AIDS patient experiencing a foreign body sensation in his left eye had a conjunctival swab tested using a calcofluor stain and a fluorescent-antibody stain with murein antiserum raised against E. hellem. A cross-reaction occured with another species of Encephalitozoon, so a PCR test was performed. It was found that the amplified rRNA generated digestion patterns by restriction endonuclease FokI that were indentical to the digestion patterns of E. hellem. These observations allowed researchers to conclude that Encephalitozoon hellem causes keratoconjunctivitis in addition to other disseminated infections in immunosuppressed patients. Doctors and researchers soon found that patients treated with albendazole and topical fumagillin responded rapidly with no opthalmologic signs

PATHOLOGYE. hellem was first isloated in HIV patients, but has

also been found to infect mice, birds, and even bats. When isolating E. hellem in the HIV patient, there were 24 monoclonal antibodies that were used against not only E. hellem, but also two other species of Encephalitozoon, E. intestinalis and E. cuniculi. The antibodies did not react with either of these two, indicating antibody specificity across the three species. Antigenic diversity of the different karyotypes of E. hellem was demonstrated as well when two monoclonal antibodies reacted with karyotype B but not with karyotype A.Experiments exposing chickens to E. hellem found that the microbe was detectable in the feces of the animals for up to 19 days, showing that E. hellem is potentially fecal borne and that chickens are a very likely host. While a definite route of infection is not well documented, it has been assumed that transmission of E. hellem most likely occurs by direct contact or by the ingestion of contaminated food or water .

Once a host has been found, E. hellem, like other microsporidia, act as spore forming parasites that use their unique polar tubule as a means of infecting their hosts. A mature, resistant spore will extrude the polar tubule and through this, the sporoplasm will be injected into the host cell. The sporoplasm is then able to multiply inside of the host cell via binary fission or multiple fission. Like the photo above illustrates, the spores will continue to multiply until the host cell cytoplasm is filled, causing it to burst and release more spores into the surroundings that will mature and carry on the infection to other cells.

Studies have found that the glycosylation of the ultrastructure gene PTP1, can be modified by O-linked mannosylation indicating that mannose pretreatment of host cells may decrease infection by E. hellem. This suggests that the O-mannosylation of PTP1 may have a functional significance for the ability of E. hellem to invade their hosts .

The clinical manifestations of E. hellem include keratoconjunctivitis, infection of respiratory and genitourinary tract, and disseminated infection. With E. hellem being one of the four most common human microsporidian parasites, hosts are usually HIV patients but infections have also been reported to infect immunodificient patients that do not have HIV.

BIOTECHNOLOGY:Encephalitozoon hellem is not known to produce any enzymes that are beneficial to the environment or its inhabitants. However, studies performed on E. hellem have shown potential to be beneficial to clinical and biological research. For example, culturing of the microbe is useful for species-species diagnosis and studying the different drug responses of each . It is also believed that different sources of E. hellem isolates could be important to finding new variants and genotyping other isolates may be important to evaluating the actual variability in the species. Also, the genotyping of this microsporidian has been helpful in understanding other forms of human microsporidosis and their transmission

RESEARCH:A recent study diagnosed a free-ranging European brown hare with chronic interstitial nephritis. The hare was infected with both E. hellem and E. intestinalis. Researchers noted wedge shaped lesions on the hare's kidneys, a symptom characterized by interstitial nephritis, most commonly associated with E. cuniculi infection. Other symptoms of the hare included dehydration, atrophic muscles, and it was severly thin. This results of this study were the first documented description of E. hellem and E. intestinalis infection in a European brown hare, this being an instance of this microsporidic infection in a non-human besides a bird. The presence of chronic interstitial nephritis in the hare suggested that E. hellem and E. intestinalis together could cause E. cuniculi-like lesions. Throughout the experiment E. hellem seemed to be more pathogenic than E. intestinalis .

Another study implemented retrospective analysis of 110 formalin-stored diarrheic stool samples from AIDS patients who suffered from intestinal microsporidiosis. These samples were taken between 1992 and 2003, and of these 2.1% had E. hellem spores present. Samples that were older than 10 years did not have as distinguished results and were deemed unsuitable for retrospective analysis . The identification of microsporidian spores using multiplex FISH assay proved to be more sensitive and give more clear results that chromotropo-2R and Calcofluor White M2R stains. Besides E. hellem, other microsporidia such as E. intestinalis were also present in the patients' samples. These results were able to show that micropsoridian co-infection was not uncommon in HIV/AIDS patients and may have contributed to a large amount of illnesses and infections that may have not been present had E. hellem existed in the body alone. Furthermore, this study found that the identification of E. hellem among other Encephalitozoon species was a useful tool for assessing spore shedding intensity in intestinal microsporidiosis and can also be used for epidemiological investigations in addition to clincal studies

The immune response to E. hellem of both the innate and and adaptive immune systems has also been recently studied. In this experiment two-day old chickens were inoculated perorally, through the mouth, and intraperitoneally, directly into the abdominal cavity, with E. hellem spores. ELISA tests were used to determine the anti-E. hellem IgY, IgA, and IgM responses in both sera and fecal samples. In the sera, the IgY was the only one measured in significant levels whereas in the fecal samples all three antibodies were present, but still with IgY being the most prevalent. More antibodies formed in the chickens that were inoculated intraperitoneally. It is possible that this occured because of the unnatural route of infection and the spores being able to directly contact the immune system and not go through intestinal barriers. This study was able to show that an E. hellem infection is asymptomatic and that spore-shedding is dependent on concurrent infection. Fecal samples of asymptomatic birds supported the assumption that the bird droppings are a potential source of infection for other hosts, such as humans. Also, based on the results on the antibody testing, the results show that immunodeficient humans infected with microsporidiosis, such as E. hellem infection, may develop parasite specific antibodies. This research could potentially help with future pharmacological advances against microsporidiosis

HENIPAVIRUSHenipavirus is a genus of the family Paramyxoviridae, order Mononegavirales containing two established species: Hendra virus and Nipah virus. The henipaviruses are naturally harboured by Pteropid fruit bats (flying foxes) and some microbat species. Henipavirus is characterised by a large genome, a wide host range, and their recent emergence as zoonotic pathogens capable of causing illness and death in domestic animals and humansIn 2009, RNA sequences of three novel viruses in phylogenetic relationship to known Henipaviruses were detected in Eidolon helvum (the African Straw-coloured fruit bat) in Ghana. The finding of these novel putative Henipaviruses outside Australia and Asia indicates that the region of potential endemicity of Henipaviruses extends to Africa.

EMERGENCEHendra virus (originally Equine morbillivirus) was discovered in September 1994 when it caused the deaths of thirteen horses, and a trainer at a training complex in Hendra, a suburb of Brisbane in Queensland, Australia.The index case, a mare, was housed with 19 other horses after falling ill, and died two days later. Subsequently, all of the horses became ill, with 13 dying. The remaining 6 animals were subsequently euthanised as a way of preventing relapsing infection and possible further transmission. Both the trainer, Victory ('Vic') Rail, and a stable hand were involved in nursing the index case and both fell ill within one week of the horse’s death with an influenza-like illness. The stable hand recovered while Mr Rail died of respiratory and renal failure. The source of the virus was most likely frothy nasal discharge from the index case.A second outbreak occurred in August 1994 (chronologically preceding the first outbreak) in Mackay 1,000 km north of Brisbane resulting in the deaths of two horses and their owner. The owner, Mark Preston, assisted in necropsies of the horses and within three weeks was admitted to hospital suffering from meningitis. Mr Preston recovered, but 14 months later developed neurologic signs and died. This outbreak was diagnosed retrospectively by the presence of Hendra virus in the brain of the patient.A survey of wildlife in the outbreak areas was conducted, and identified pteropid fruit bats as the most likely source of Hendra virus, with a seroprevalence of 47%. All of the other 46 species sampled were negative. Virus isolations from the reproductive tract and urine of wild bats indicated that transmission to horses may have occurred via exposure to bat urine or birthing fluids

Events of June – August 2011In the years 1994–2010, fourteen events were recorded. Between 20 June 2011 and 28 August 2011, a further seventeen events were identified, during which twenty-one horses died.It's not clear why there has been a sudden increase in the number of spillover events between June and August 2011. Typically HeV spillover events are more common between May and October. This time is sometimes called "Hendra Season". This is a time when there are large numbers of fruit bats of all species congregated in SE Queensland as this area contains valuable winter foraging habitat. The weather (warm and humid) is favourable to the survival of henipavirus in the environment.There have been suggestions that the flooding that affected SE Queensland and Northern NSW in December 2010 and January 2011 may be having an impact upon the health of the fruit bats. Urine sampling in flying-fox camps indicate that a larger proportion of flying-foxes than usual are shedding live virus. Biosecurity Queensland's ongoing surveillance usually shows 7% of the animals are shedding live virus. In June and July nearly 30% animals have been reported to be shedding live virus. Present advice is that these events are not being driven by any mutation in HeV itself.Other suggestions include that an increase in testing has led to an increase in detection. As the actual mode of transmission between bats and horses has not been determined, it is not clear what, if any, factors can increase the chance of infection in horses.Following the confirmation of a dog with HeV antibodies, on 27 July 2011, the Queensland and NSW governments will boost research funding into the Hendra virus by $6 million to be spent by 2014/2015. This money will be used for research into ecological drivers of infection in the bats and the mechanism of virus transmission between bats and other species. A further 6 million dollars was allocated by the federal government with the funds being split, half for human health investigations and half for animal health and biodiversity research

PathologyFlying foxes experimentally infected with the Hendra virus develop a viraemia then excrete the virus in their urine, faeces and saliva for approximately one week. Although they excrete live virus during this time there is no other indication of an illness. Symptoms of Hendra virus infection of humans may be respiratory, including hemorrhage and edema of the lungs, or encephalitic, resulting in meningitis. In horses, infection usually causes pulmonary oedema, congestion and / or neurological signs.

Ephrin B2 has been identified as the main receptor for the henipaviruses

VaccineA subunit vaccine that will neutralise Hendra virus is in development and is expected to be available in 2013. It is composed of a soluble version of the G surface antigen on Hendra virus and has been successful in ferret models. The trial vaccine may be available in 2012.The vaccine is intended to be used in horses as stopping the virus at this point should protect both horses and humans.

NIPA VIRUSEMERGENCENipah virus was identified in April 1999, when it caused an outbreak of neurological and respiratory disease on pig farms in peninsular Malaysia, resulting in 257 human cases, including 105 human deaths and the culling of one million pigs. In Singapore, 11 cases, including one death, occurred in abattoir workers exposed to pigs imported from the affected Malaysian farms. The Nipah virus has been classified by the Centers for Disease Control and Prevention as a Category C agent.[ The name "Nipah" refers to the place, Kampung Baru Sungai Nipah in Negeri Sembilan State, Malaysia, the source of the human case from which Nipah virus was first isolated.The outbreak was originally mistaken for Japanese encephalitis (JE), however, physicians in the area noted that persons who had been vaccinated against JE were not protected, and the number of cases among adults was unusual [78]

 Despite the fact that these observations were recorded in the first month of the outbreak, the Ministry of Health failed to react accordingly, and instead launched a nationwide campaign to educate people on the dangers of JE and its vector, Culex mosquitoes.Symptoms of infection from the Malaysian outbreak were primarily encephalitic in humans and respiratory in pigs. Later outbreaks have caused respiratory illness in humans, increasing the likelihood of human-to-human transmission and indicating the existence of more dangerous strains of the virus.

Based on seroprevalence data and virus isolations, the primary reservoir for Nipah virus was identified as Pteropid fruit bats, including Pteropus vampyrus(Large Flying Fox), and Pteropus hypomelanus (Small Flying-fox), both of which occur in Malaysia.The transmission of Nipah virus from flying foxes to pigs is thought to be due to an increasing overlap between bat habitats and piggeries in peninsular Malaysia. At the index farm, fruit orchards were in close proximity to the piggery, allowing the spillage of urine, faeces and partially eaten fruit onto the pigs.[79] Retrospective studies demonstrate that viral spillover into pigs may have been occurring in Malaysia since 1996 without detection. During 1998, viral spread was aided by the transfer of infected pigs to other farms, where new outbreaks occurred.

PathologyIn humans, the infection presents as fever, headache and drowsiness. Cough, abdominal pain, nausea, vomiting, weakness, problems with swallowing and blurred vision are relatively common. About a quarter of the patients have seizures and about 60% become comatose and might need mechanical ventilation. In patients with severe disease, their conscious state may deteriorate and they may develop severe hypertension, fast heart rate, and very high temperature.Nipah virus is also known to cause relapse encephalitis. In the initial Malaysian outbreak, a patient presented with relapse encephalitis some 53 months after his initial infection. There is no definitive treatment for Nipah encephalitis, apart from supportive measures, such as mechanical ventilation and prevention of secondary infection. Ribavirin, an antiviral drug, was tested in the Malaysian outbreak, and the results were encouraging, though further studies are still needed.In animals, especially in pigs, the virus causes a porcine respiratory and neurologic syndrome, locally known as "barking pig syndrome" or "one mile cough."Ephrin B2 has been identified as the main receptor for the henipaviruses

Causes of emergenceThe emergence of henipaviruses parallels the emergence of other zoonotic viruses in recent decades. SARS coronavirus, Australian bat lyssavirus, Menangle virus and probably Ebola virus and MarburG virus are also harbored by bats and are capable of infecting a variety of other species. The emergence of each of these viruses has been linked to an increase in contact between bats and humans, sometimes involving an intermediate domestic animal host. The increased contact is driven both by human encroachment into the bats’ territory (in the case of Nipah, specifically pigpens in said territory) and by movement of bats towards human populations due to changes in food distribution and loss of habitat.There is evidence that habitat loss for flying-foxes, both in South Asia and Australia (particularly along the east coast) as well as encroachment of human dwellings and agriculture into the remaining habitats, is creating greater overlap of human and flying fox distributions.

THE END

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