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The Present Status of Schistosomiasis Control in Morocco *
Published in Max J. Miller, E. J. Love, Parasitic Diseases: Treatment and Control, 2020
The parasite load: several thousand cases were notified every year — 3036 in 1976, 5295 in 1976.3 More than 80% of these cases were from the southern provinces. Children less than 14 years old were the most affected group (i.e., 65% of all reported cases).4 Surveys demonstrated that 90% of the cases detected had a parasite count of less than 50 eggs per ml of urinary sediment examined.5
Strongyloidiasis
Published in Peter D. Walzer, Robert M. Genta, Parasitic Infections in the Compromised Host, 2020
Robert M. Genta, Peter D. Walzer
A number of factors, however, make the parasitological diagnosis of strongyloidiasis a uniquely challenging task. Although no human data are available, animal studies suggest that in chronic, asymptomatic infections (such as those found in most patients) the parasite load may be relatively small. Another factor that contributes to limit the number of fecal larvae is the low rate of egg production by the S. stercorals female. It has been estimated that no more than 50 eggs per day are passed by each adult worm, in sharp contrast with other intestinal nematodes such as Ascaris lumbricoides, whose female may pass up to 1 million eggs a day (263). In addition, these few eggs are apparently produced rather irregularly (14), and this may result in the uneven distribution of larvae in the fecal matter. Because of this, the sampling error may be great, and the chances of finding lame in the small quantity of feces usually examined in a clinical parasitology laboratory may be very slim. Finally, the peculiar ability of S, stercoralis larvae to repenetrate the intestinal mucosa may further reduce the number of fecal larvae. In fact, we have observed immunosuppressed monkeys with severe infections consisting of over 300,000 adult worms that on certain days would have negative stools (30). In those circumstances, it is possible that all larvae were repenetrating through the colonic mucosa and none were passed out with the feces. Necropsy findings confirmed the presence of heavy mucosal penetration in the colon.
Tropical Colorectal Surgery
Published in Peter Sagar, Andrew G. Hill, Charles H. Knowles, Stefan Post, Willem A. Bemelman, Patricia L. Roberts, Susan Galandiuk, John R.T. Monson, Michael R.B. Keighley, Norman S. Williams, Keighley & Williams’ Surgery of the Anus, Rectum and Colon, 2019
Meheshinder Singh, Kemal I. Deen
Damage to the host is believed to occur largely as a result of direct invasion of the parasite into the intestinal mucosa. Secondary bacterial colonisation is thought to occur at sites where there is a breach in the colonic mucosa and also during heavy infection. Severe mucosal damage may produce overt ulceration of the colonic mucosa leading to loss of blood and protein. Blood loss in children has been shown to be proportional to the parasite load. Although it has been estimated that a single worm causes a loss of only 0.005 mL/day, chronic infestation with a high worm load can produce anaemia, particularly in an already nutritionally compromised individual. The associated inflammatory response, which includes lymphocytes, plasma cells and occasionally eosinophils, may contribute to exudative losses from the colon.
Molecular diagnosis of toxoplasmosis: recent advances and a look to the future
Published in Expert Review of Anti-infective Therapy, 2021
Marie Gladys Robert, Marie-Pierre Brenier-Pinchart, Cécile Garnaud, Hélène Fricker-Hidalgo, Hervé Pelloux
The introduction of quantitative real-time PCR techniques in diagnosis has enabled the determination of the parasite load in the AF, which could be relatively low [27]. A correlation between parasite load and clinical signs has also been investigated. Costa et al. suggested that a high parasite count tended to be associated with ultrasonographic abnormality, even if the main contribution factor remained early maternal infection [27]. Romand et al. showed that maternal infections acquired before 20 weeks with a parasite load greater than 100 parasites/mL of AF had the highest risk of severe fetal outcomes while Yamamoto et al. also noticed an association between parasite load and clinical outcomes but regardless of the gestational age at the time of maternal infection [28,29]. However, the influence of parasitic load on fetal prognosis is still debated. Quantification is not standardized and still shows significant variations between laboratories [30]. Only the qualitative results are therefore generally released, and to date, the management of CT do not depend on this parasite load.
Animal models of Chagas disease and their translational value to drug development
Published in Expert Opinion on Drug Discovery, 2020
Trypanosoma cruzi spreads primarily through blood-sucking triatomine bugs, but other modes of transmission, such as congenital transmission from mother to child or transmission through contaminated food or drink, are gaining in importance; other potential routes of infection include blood transfusion, organ transplantation, accidental contact in research laboratories, and sexual transmission [13,14,15]. The disease has two clinically defined phases [16,17]: an acute disease phase that occurs 2–8 weeks post-infection, characterized by elevated parasite load. Symptoms during this period are normally mild, although lethal outcomes may occur in 5% of diagnosed cases, and bloodstream parasites are easily detectable by microscopy.A strong adaptive immune response brings the parasite load down to low/undetectable levels that last throughout the infection. Infected individuals enter the so-called indeterminate phase of the chronic stage; the majority remain asymptomatic during their entire life, while around 30–40% of those infected eventually develop clinical manifestations such as cardiomyopathy or digestive tract megasyndromes such as megacolon or both. Progressive heart failure and sudden death remain the main causes of death for these patients [18].
The enemy at home: leishmaniasis in the Mediterranean basin, Italy on the focus
Published in Expert Review of Anti-infective Therapy, 2020
Elena Gianchecchi, Emanuele Montomoli
Poverty, malnutrition, youth, elevated parasite load and immune deficiency constitute the main risk factors [134]. Immunosuppression is a well-known factor for VL onset. Increasing concern regards the emergence of VL as an opportunistic infection not only in subjects characterized by an impaired cell-mediated immunity [135] due to human immunodeficiency infection [136], but also in individuals presenting a secondary immunosuppression [40,127,137,138]. The clinical presentation of VL in immunosuppressed patients can be atypical, involving essentially any organ system and the severity is enhanced. More specifically, they do not show specific symptoms, some common manifestations of VL, such as splenomegaly, may be more subtle or absent, fever can be absent, and they can manifest only weight loss and pancytopenia. In addition, patients with HIV-associated VL can present quite commonly localized or diffuse dermatologic or mucosal involvement [137].