But of course this is a flaw of more experienced movie-makers as well. In the end, there is a big "revelation" which I won't blow, but which makes absolutely no sense for a kid to have had as a secret. And the revelation keeps going on and on in a breathless "isn't this cool" idea which is just like what you'd expect from a teenage girl.
I applaud her effort even if it is mostly just a curiosity! So atta girl! Was this review helpful? Sign in to vote. It was a very good experience, mainly because of the documentary. After the movie session the audience had a very enlightening talk with 3 horror-movies specialists.
Technically speaking, this movie is terrible. It is full of continuity problems, including sequences where the time of the day changes from one scene to the other, with a dialog starting in daylight and continuing in a night-dark environment, then going back to a daylight environment, all in the same conversation of the characters. The sound is sometimes inaudible, but most of the time it's just bad.
The actors are completely amateur, being a group of Emily's school colleagues. If you are into "B" movies for the fun of its mistakes, you'll love this movie. There are 2 good things about this movie. An infection which appears to be caused by a bacteria in the water turns out to be more.
A fourteen-year-old student, Dannie, feels the real cause is linked to her recurring dreams. When the infection reaches an epidemic level. This unique twist on the classic zombie theme, centers around the highly-intuitive Dannie Jacobs and a group of four other middle school students who try to save their friends, their town and themselves in spite of the odds against them.
While they are desperately trying to find an answer before it's too late, they meet researcher Sue who may hold the key to the infection and Dannie's dreams.
Research gone awry results in a host of zombies walking the streets of Austin. Read all An infection which appears to be caused by a bacteria in the water turns out to be more. When the infection reaches an epidemic level. Read all. Director Emily Hagins. Emily Hagins. Top credits Director Emily Hagins. See more at IMDbPro. Photos Add photo. Top cast Edit. Alec Herskowitz Sam as Sam. Tiger Darrow Christine as Christine. Tony Vespe Cameron as Cameron. Alex Schroeder Stacy as Stacy.
Estrella Gonzales Jen as Jen. Amanda Haight Chloe as Chloe. Jose Ramirez Doctor as Doctor. Jessica Cargill Researcher as Researcher. Robert Cargill Janitor as Janitor. Joy M. Virulence among E. For instance, glycosidases such as sialidase, N-acetylgalactosamidase, and N-acetylglucosaminidase are needed to remove the branched polysaccharides from mucin cells [ 15 ]. This allows the trophozoites to degrade the protective mucous barrier and subsequently penetrate the colonic epithelium increasing the risk of metastasis to distant sites [ 15 ].
In a transcriptone analysis study, virulence of E. Species lacking this enzyme were unable to breach the mucus barrier and cause invasive disease [ 15 , 16 ]. Other mechanisms involved in the killing of the epithelial cells and inflammatory cells, including secretion of proteinases cysteine proteinase , contact-dependent target cells lysis, apoptosis and the formation of amebapores causing cytolysis of infected cells [ 1 , 7 , 15 , 16 ].
Several hypotheses have been posited to explain why certain patients have asymptomatic disease, while others progress to invasive disease and are currently being tested. Strain virulence, environment, and the host's genetic susceptibility, immune status, age, and gender have all been found to predict disease severity [ 1 , 5 , 9 ]. Recent studies have shown that the interaction between the host's intestinal flora and E.
Production of proinflammatory cytokines was also augmented in the presence of certain gut bacteria, causing further epithelial damage and facilitating trophozoite invasion [ 20 ].
The production of mucosal immunoglobulins Ig , particularly secretory IgA, plays an important role in the host's gut immune response. Secretory IgA is secreted by plasma cells within the lamina propia and aid in preventing pathogens from adhering and penetrating the mucosal barrier. Another recent study conducted by Bernin and colleagues [ 9 ] analyzed and compared the sera of patients with ALA, asymptomatic carriers of E.
They found that patients with ALA and asymptomatic carriers both had high titers of IgG and all its subclasses, as well as IgA, suggesting that a strong immune reaction takes place in asymptomatic carriers.
Furthermore, sex specific analyses revealed that female asymptomatic carriers had significantly higher titers of IgG and IgG1 subclass in comparison to male asymptomatic carriers [ 9 ].
This strong complement-mediated mechanism may be another factor responsible for the decreased prevalence of ALA in the female population [ 9 ]. The Entamoeba dispar species is morphologically similar to E. Until recently, emerging reports have demonstrated the presence of E. Using molecular DNA sequencing and genotyping of different E.
Various in vivo and in vitro studies [ 17 — 19 ] also show that cultural and environmental factors play a significant role in the pathogenic behavior of various E. Dolabella and colleagues [ 17 ] hypothesized that coinfection with both E. Given the small number of studies, the pathogenic potential of E.
Further research is needed because treatment will be indicated for infected patients if E. Approximately ninety percent of Entamoeba infections are asymptomatic [ 1 , 2 , 10 ]. Risk factors that are associated with increased disease severity and mortality include young age, pregnancy, malignancy, malnutrition, alcoholism, and corticosteroid use [ 10 , 11 ]. Amoebic colitis generally has a subacute onset, with symptoms that can range from mild diarrhea to severe dysentery, with abdominal pain and watery or bloody diarrhea [ 1 ].
Symptoms tend to be nonspecific and the differential diagnosis is broad. Infectious causes that need to be excluded include shigella, salmonella, campylobacter, and enteroinvasive and enterohemorrhagic Escherichia coli [ 1 , 25 ].
Noninfectious causes include inflammatory bowel disease, intestinal tuberculosis, diverticulitis, and ischemic colitis [ 25 ]. Unusual but serious complications such as fulminant necrotizing colitis, toxic megacolon, and fistulizing perianal ulcerations can occur, especially when diagnosis and treatment is not timely [ 1 , 26 , 27 ]. These patients appear toxic, with fever, bloody diarrhea, and signs of peritoneal irritation [ 26 , 30 ].
The development of toxic megacolon has been linked to corticosteroid use and is unresponsive to antiamoebic therapy, requiring immediate surgical intervention [ 30 , 31 ]. Exclusion of inflammatory bowel disease is exceptionally important, given that misdiagnosis and treatment with corticosteroids can lead to these serious complications.
The formation of an ameboma is another uncommon manifestation that may occur in amebic colitis. It tends to present with pain and swelling in the right iliac fossa, or with symptoms of bowel obstruction [ 27 , 32 ]. Macroscopically, amebomas resemble a mass or multiple masses typically localized in the cecum or ascending colon and consist of localized hyperplastic granulation tissue [ 27 , 32 ].
Ameboma formation has been generally associated with untreated or partially treated amoebic colitis [ 27 ]. Given that its appearance can resemble lymphoma, neoplasm, tuberculosis, abscess, or inflammatory bowel disease, colonoscopy and histopathological examination of the biopsied material are warranted to exclude other sinister lesions [ 27 , 30 ].
Amebic liver abscess is the most common extra intestinal manifestation of amoebiasis [ 7 ]. Cough, right-sided pleural pain, and subsequent pleural effusion may occur when the diaphragmatic surface of the liver is involved [ 1 ]. Leukocytosis, transaminitis, and elevated alkaline phosphatase on laboratory evaluation are usually present and imaging reveals an abscess, typically on the right hepatic lobe [ 7 , 11 ]. Amoebic abscesses tend to be solitary, but multiple abscesses can occur and have been described in previous literature [ 34 , 35 ].
Anemia and hypoalbuminemia are very common in ALA in comparison to pyogenic abscesses [ 34 ]. The lungs are the second most common extra intestinal organ affected [ 36 ]. Pulmonary amoebiasis generally occurs by direct extension of an ALA but can also occur by direct hematogenous spread from intestinal lesions or by lymphatic spread [ 36 , 37 ]. The right lower or middle lobe of the lung is most commonly affected. Patients present with fever, hemoptysis, right upper quadrant pain, and referred pain to the right shoulder or intrascapular region.
Pulmonary abscesses, bronchohepatic fistula, and empyema can occur when a liver abscess ruptures into the pleural space [ 36 ]. The presence of bile in these secretions indicates liver origin [ 36 ]. Rupture of the liver abscess into the pericardium is also a rare complication with high mortality [ 38 ].
It can present acutely with cardiac tamponade resulting from purulent pericarditis, or with a slowly accumulating pericardial effusion.
Symptoms include severe chest pain, shortness of breath, and edema from congestive heart failure or constrictive pericarditis [ 38 ].
Mechanical compression of the IVC by a large hepatic abscess or by erosion from a posterior liver abscess can lead to embolism of the IVC and thromboembolic disease of the lungs [ 36 , 39 ].
The World Health Organization WHO ranks diarrheal disease as the second most common cause of morbidity and mortality in children in the developing countries [ 40 ]. In , the WHO stated the necessity to diagnose and treat all infections with E. Various diagnostic tools exist for the diagnosis of E.
Identification of cysts or trophozoites in stool cannot accurately identify the disease caused by E. The identification of E.
It has high sensitivity and specificity; however, due to lack of standardization and high cost, it is not yet widely available for diagnostic testing [ 41 ]. Stool and serum antigen detection assays are sensitive, specific differentiating between strains , and easy to preform and can potentially diagnose early infection [ 42 ].
These assays use monoclonal antibodies to bind to epitopes found on E. Unlike E. Finally, direct visualization of the colon by colonoscopy can be performed to diagnose amoebiasis, particularly when nonspecific gastrointestinal symptoms make diagnosis difficult [ 44 ]. It is also useful in excluding other disease, particularly neoplasms. The diagnostic value of the colonoscopy lies in the ability to take biopsies and microscopically identify intestinal amoebiasis.
Lee and colleagues [ 44 ] found right-sided colitis and proctosigmoiditis varied in colonoscopic appearance. Right-sided disease included erosions, ulcers, exudates, or edematous cecal mucosa, while findings for proctosigmoiditis were swollen, edematous mucosa with bloody exudate [ 44 ]. Intestinal tuberculosis and inflammatory bowel disease can present similar to amoebic colitis.
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