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The Small Intestine
Published in Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie, Bailey & Love's Short Practice of Surgery, 2018
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie
The course of CD after surgery is unpredictable, but recrudescence (a better term than ‘recurrence’, as surgery never cures CD) is common. Symptomatic recrudescence does not seem to be related to the presence of disease at the resection line. The cumulative probability of recrudescence requiring surgery for ileal disease is approximately 20, 40, 60 and 80% at 5, 10, 15 and 20 years, respectively, after a previous resection.
Virus
Published in Joseph R. Masci, Elizabeth Bass, Ebola, 2017
Joseph R. Masci, Elizabeth Bass
Two health care workers who had traveled to the endemic area during the 2014–2016 epidemics were documented to have persistent infection in two unexpected places: the central nervous system and the eye. The presence of Ebola virus was found by PCR in the cerebrospinal fluid (CSF) of a patient who had recovered from viremia (Howlett et al. 2016) in Sierra Leone. Similarly, high levels of virus were detected in the CSF more than nine months after recovery from acute EVD (BBC 2015). In the other patient, virus was isolated from the vitreous three months after recovery from acute infection. Both of these health care workers had received immunotherapy during their acute infections. This has raised the concern that this form of therapy may increase the likelihood of persistence of infection in these sites and of clinical recrudescence (Fischer and Wohl 2016).
Plasmodium malariae and Plasmodium ovale
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2015
Eric S. Loker, Bruce V. Hofkin
Pathology Infections caused by P. malariae and P. ovale are much less severe than for P. vivax and especially P. falciparum. Tertian malaria caused by P. ovale, like that caused by P. vivax, results in fever paroxysms every 48 hours, corresponding to the rupture of infected erythrocytes and the release of merozoites. Furthermore, sporozoites infecting liver cells do not necessarily undergo schizogony but may form hypnozoites, which may result in a relapse of disease up to 20 months after the initial infection. The slower growing P. malariae causes disease with paroxysms every 72 hours, known as quartan malaria. Although it does not enter a latent, hypnozoite stage, P. malariae can persist at low, subclinical levels for many years in infected individuals, who serve as reservoirs. It can later reach clinical significance again, a phenomenon known as recrudescence.
Trachoma elimination in Togo: lessons and recommendations for African countries
Published in Pathogens and Global Health, 2023
Taiwo Oluwaseun Sokunbi, Vishnu Unnithan, Brigid Unim, Janice Odhiambo, Zakariya’u Dauda, Fortune Benjamin Effiong
Global efforts to combat Trachoma have employed the use of ‘Surgery, Antibiotics, Facial cleanliness, and Environmental improvement’ (SAFE) and ‘Water, Sanitation, and Handwashing’ (WASH) strategies [1,4]. Mass drug administration with azithromycin has also been recommended for community control of trachoma [4]. Although progress has been made with endemic districts managing to sustain lower prevalence rates, recrudescence has been a concern. The disease was targeted by the World Health Organization (WHO) for global elimination by 2020. However, this has not been achieved yet, and 2030 has been set as the new target date [1].
The gamma-aminobutyric acid-B receptor (GABAB) encephalitis: clinical manifestations and response to immunotherapy
Published in International Journal of Neuroscience, 2018
Junzhao Cui, Hui Bu, Junying He, Zeyan Zhao, Weixin Han, Ruiping Gao, Xiaoqing Li, Qing Li, Xiaosu Guo, Yueli Zou
There is no standard care for LE and the response varies. However, most experts agree on the use of immunotherapies. One of the suggested guideline is using high doses of corticosteroid, intravenous immunoglobulin and plasmapheresis (plasma exchange, immunoadsorption) as first-line therapy and adding rituximab and cyclophosphamide as second-line therapies in refractory cases [3]. Recently, it has been shown that seizures caused by anti-GABAB receptor encephalitis are often resistant against anti-epileptic drugs and respond well to immunotherapies [22]. In addition, previous reports have demonstrated that combination therapy might be superior to monotherapy in decreasing the rate of recrudescence, improving the degree of recovery [23]. Response to therapy is best judged by the patient's clinical status. In our research, five patients received combination treatment of corticosteroids and immunoglobulins, four of whom had a favorable prognosis, with mRS scores of 1 (cases 4, 5 and 6) and 2 (case 11), the rest one (case 10) died of status epilepticus on follow-up at 6 months. Furthermore, for patients with tumors, treatment of cancer may also be necessary. In our study, all SCLC patients timely received pneumonectomy and/or postoperative radiochemotherapy after diagnosis, four of whom had achieved a neurological relief after immunotherapy and anti-neoplastic treatment at the end of follow-up ranging from 7 to 15.25 months. The incidence of GABAB encephalitis is low, and the case reports of the treatment of the diseases are poor [7,10]. Studies have shown that patients with GABAB encephalitis have better outcomes if they received immunotherapy at earlier stages of the disease than those who did not [24]. Therefore, it is strongly suggested that the therapy should be initiated once the autoantibodies are detected in serum or CSF.
Stroke mimics: incidence, aetiology, clinical features and treatment
Published in Annals of Medicine, 2021
Brian H. Buck, Naveed Akhtar, Anas Alrohimi, Khurshid Khan, Ashfaq Shuaib
Recrudescence refers to the re-emergence of the previous stroke-related deficits in the settings of metabolic, infectious and toxic dysfunction. The diagnosis requires an MRI which shows the old stroke and reveals no new DWI-MRI deficits. Symptoms are mostly short-lived and show improvement within 24 h in most subjects. Recrudescence can develop within weeks to years after the previous stroke [11]. The recrudescence under metabolic, infection, fatigue or sedative medications is likely due to functional suppression of compensatory cerebral networks [78].