Waterborne zoonoses *
Jamie Bartram, Rachel Baum, Peter A. Coclanis, David M. Gute, David Kay, Stéphanie McFadyen, Katherine Pond, William Robertson, Michael J. Rouse in Routledge Handbook of Water and Health, 2015
Oocysts of the organism are widely distributed in both the terrestrial and aquatic environments. It has a low infectious dose (as few as 10 oocycts) and is highly resistant to chlorine and other bactericidal agents used for disinfection and water treatment. The resistance of the oocycts to these agents explains how outbreaks of gastrointestinal illness associated with treated drinking water and swimming pools and waterparks occur. In the developed world, large outbreaks of waterborne cryptosporidiosis have been associated with failures of water treatment systems or high loads of oocysts that result from flooding or overt fecal contamination of water sources that overwhelm water treatment systems. Fortunately, cryptosporidia are sensitive to UV light disinfection procedures.
Cystoisospora belli
Dongyou Liu in Laboratory Models for Foodborne Infections, 2017
Developmental stages of Cystoisospora comprise asexual multiplication, sexual reproduction, and sporogony. The life cycle of C. belli completes within the human host without known animal reservoirs. Humans get infected by ingestion of food or water contaminated with oocysts (Figure 38.2). The infective stage of C. belli is characterized by an oval or rugby-shaped oocyst with a wide range of size variation in terms of the maximum length and width, both within and between isolates. The average length measured from more than 700 oocysts is 28.3 μm (range = 17–37). A remarkable narrowing with a neck-like appearance may be observed at one end of some oocysts, whereas most oocysts are nearly symmetric at both ends. The maximum width of oocysts averages 13.5 μm (range = 8–21). The mean shape index or the ratio of length to width of oocysts is 2.1 (range = 1.3–3.3) [9]. The oocyst wall is bilayer, thin, smooth, and transparent for all stages of development. The inner wall is membranous, and the outer wall is rigid and relatively impermeable to external fluids [16]. When freshly passed in feces, the oocyst remains immature, containing a spherical or slightly elongated, oval-shaped sporoblast that develops within another rigid cyst wall called sporocyst. Occasionally, some freshly passed oocysts in stool may contain two sporocysts, each of which possesses one sporoblast. The sporocyst of C. belli lacks a proteinaceous plug, known as a Stieda body, a structure existing in the genus Isospora. The dimension of sporocyst is 12–14 μm × 7–9 μm.
Cystoisospora belli
Dongyou Liu in Handbook of Foodborne Diseases, 2018
Developmental stages of Cystoisospora comprise asexual multiplication, sexual reproduction, and sporogony. The life cycle of C. belli completes within the human host without known animal reservoirs. Humans get infected by ingestion of food or water contaminated with oocysts (Figure 54.3). The infective stage of C. belli is characterized by an oval or rugby-shaped oocyst with a wide range of size variation in terms of the maximum length and width, both within and between isolates. The average length measured from more than 700 oocysts is 28.3 μm (range = 17–37). A remarkable narrowing with a neck-like appearance may be observed at one end of some oocysts, whereas most oocysts are nearly symmetric at both ends. The maximum width of oocysts averages 13.5 μm (range = 8–21). The mean shape index or the ratio of length-to-width of oocyst is 2.1 (range = 1.3–3.3) [9]. The oocyst wall is bilayer, thin, smooth, and transparent for all stages of development. The inner wall is membranous, and the outer wall is rigid and relatively impermeable to external fluids [16]. When freshly passed in feces, the oocyst remains immature, containing a spherical or slightly elongated, oval-shaped sporoblast that develops within another rigid cyst wall called “sporocyst.” Occasionally, some freshly passed oocysts in stool may contain two sporocysts, each of which possesses one sporoblast. The sporocyst of C. belli lacks a proteinaceous plug, known as a Stieda body, a structure existing in the genus Isospora. The dimension of sporocyst is 12–14 μm × 7–9 μm.
A review on inactivation methods of Toxoplasma gondii in foods
Published in Pathogens and Global Health, 2018
Adel Mirza Alizadeh, Sahar Jazaeri, Bahar Shemshadi, Fataneh Hashempour-Baltork, Zahra Sarlak, Zahra Pilevar, Hedayat Hosseini
T. gondii cannot grow outside of a suitable host, in all food types or in other environments; however, findings have shown that T. gondii infection can be transmitted by the ingestion of oocysts (from contamination of the environment through cat feces) and can contaminate drinking or surface water, soil (an oocyst can survive in soil for up to two years) [2] and fruits and vegetables or by viable tissue cysts found in raw or undercooked meat of intermediate hosts (all warm-blooded animals, including most livestock and humans) [3,4]. The oocysts are highly infectious to herbivores, as are the bradyzoites to cats. There are three infectious stages of T. gondii: in groups or clones as a tachyzoites, in tissue cysts as a bradyzoites and in oocysts as sporozoites. Biological life cycle of T. gondii is classified in the sexual and asexual stages. The sexual cycle is restricted to the feline intestine and lead to shedding of oocysts in cat feces. The activated oocysts (excretion by cat) become extremely infectious and can survive in the environment for long time (several months) and possibly years. The asexual cycle is initiated when any other warm-blooded animal ingests these infectious oocysts [5].
4-Arylthiosemicarbazide derivatives as a new class of tyrosinase inhibitors and anti-Toxoplasma gondii agents
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2021
Adrian Bekier, Lidia Węglińska, Agata Paneth, Piotr Paneth, Katarzyna Dzitko
T. gondii exists in three infectious stages, such as oocysts (with sporozoites), tissue cysts (with bradyzoites), and rapidly proliferated tachyzoites, which form the parasitophorous vacuole (PV), a structure created by apicomplexan parasites in the host cells. Oocysts are only produced in the definitive hosts – members of the Felidae family (domestic cats and their relatives). Unsporulated oocysts are excreted in feline faeces of infected individuals. Each sporulated oocyst contains two sporocysts which hold four sporozoites. Even if a single sporulated oocyst is ingested or inhaled by the intermediate host, including all classes of warm-blooded vertebrates, sporozoites transform to tachyzoites, which localised in neural and muscle tissues including brain, eye, skeletal muscle, kidney, spleen, blood, liver, and heart tissue, and convert to bradyzoites enclosed in cysts that persist chronically10. In the case of infected pregnant women, tachyzoites can penetrate into the foetus via the bloodstream or placenta during the acute phase or reactivation of the infection. Ingestion of the tissue cysts in contaminated meat is also a source of infection, as bradyzoites transform back into tachyzoites upon entering a new host11.
Novel treatment strategies and drugs in development for cryptosporidiosis
Published in Expert Review of Anti-infective Therapy, 2018
Miguel A Chavez, A Clinton White
Statins are widely used for cardiovascular disease and are known to inhibit 3-hydroxy-3-methyl-glutaryl CoA (HMG-CoA) reductase, which converts HMG-CoA into mevalonic acid thus inhibiting synthesis of cholesterol [23]. In addition, mevalonic acid can produce isoprenylated proteins. Cryptosporidium spp. have been found to possess multiple metabolic pathways that utilize isoprenoids [24]; however, they lack all known enzymes to synthesize isoprenoid precursors and thus depend on host production for these proteins [25,26]. Bessoff et al. in screening drug libraries identified itavastatin as a potent inhibitor of C. parvum growth in in vitro models [25]. Madbouly Taha et al. tested atorvastatin alone or in combination with nitazoxanide against Cryptosporidium in a study using dexamethasone-treated mice [26]. The number of oocysts was lower in both intestinal contents and fecal material with the combination. Similarly, significant improvement was noted on histopathological changes in the small bowel with combined therapy as compared to the untreated infected group. They concluded that the combination of atorvastatin and nitazoxanide showed a synergistic effect on Cryptosporidium spp. infection in the intestines on immunosuppressed mice and was superior to either treatment alone. Given atorvastatin’s well-known safety profile and common use for treatment of hypercholesterolemia and cardiovascular disease, combination with nitazoxanide might prove to be an alternative treatment for cryptosporidiosis.
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