Background: Schistosomiasis is the second major human parasitic disease next to malaria, in terms of socioeconomic and public health consequences, especially in sub-Saharan Africa. Schistosoma haematobium (S. haematobium) is a trematode and one of the species of Schistosoma that cause urogenital schistosomiasis (urinary schistosomiasis). Although the knowledge of this disease has improved over the years, there are still endemic areas, with most of the reported cases in Africa, including Ghana. Not much has been done in Ghana to investigate cytological abnormalities in individuals within endemic communities, although there are epidemiologic evidences linking S. haematobium infection with carcinoma of the bladder.
Aim: The aim of this study was to identify microscopic and cytological abnormalities in the urine deposits of S. haematobium-infected children.
Methodology: Three hundred and sixty-seven (367) urine samples were collected from school children in Zenu and Weija communities. All the samples were examined microscopically for the presence of S. haematobium eggs, after which the infected samples and controls were processed for cytological investigation.
Results: S. haematobium ova were present in 66 (18.0%) out of the 367 urine samples. Inflammatory cells (82%, 54/66), hyperkeratosis (47%, 31/66), and squamous cell metaplasia (24%, 16/66) were the main observations made during the cytological examination of the S. haematobium-infected urine samples.
Conclusion: Cytological abnormalities in S. haematobium-infected children may play an important role in the severity of the disease, leading to the possible development of bladder cancer in later years, if early attention is not given. Therefore, routine cytological screening for urogenital schistosomiasis patients (especially children) at hospitals in S. haematobium-endemic locations is recommended.
This article addresses the recent use of mathematical epidemiological SIR or SEIR models in plague research. This use of S(E)IR models is highly problematic, but the problems are not presented and considered. Serious problems show in that such models are used to "prove" that historical plague was a (1) Filoviridae disease and (2) a bacterial disease caused by Yersinia pestis which was transmitted by human fleas and lice. (3) They also support early-phase transmission (by fleas). They purportedly consistently disprove (4) the conventional view that plague is/was a rat-and-rat-flea-borne disease. For these reasons, the focus is on methodological problems and on empirical testing by modern medical, entomological, and historical epidemiological data. An important or predominant vectorial role in plague epidemics for human fleas and lice requires that several necessary conditions are satisfied, which are generally not considered by advocates of the human ectoparasite hypothesis of plague transmission: (1) the prevalence and levels of human plague bacteraemia (human plague cases as sources of infection of feeding human ectoparasites); (2) the general size of blood meals ingested by human fleas and lice; (3) the consequent number of ingested plague bacteria; (4) the lethal dose of bacteria for 50% of a normal sample of infected human beings, LD50; and (5) efficient mechanism of transmission by lice and by fleas. The factual answers to these crucial questions can be ascertained and shown to invalidate the human ectoparasite hypothesis. The view of the standard works on plague has been corroborated, that bubonic plague, historical and modern, is/was a rat-and-rat-flea-borne disease caused by Yersinia pestis. These conclusions are concordant with and corroborate recent studies which, by laboratory experiments, invalidated the early-transmission hypothesis as a mechanism of transmission of LDs to humans in plague epidemics and removed this solution to the problem of transmission by human fleas.
Background and objective: Haemophilus influenzae (HI) is a common cause of community-acquired pneumonia in children. In many countries, HI strains are increasingly resistant to ampicillin and other commonly prescribed antibiotics, posing a challenge for effective clinical treatment. This study was undertaken to determine the antibiotic resistance profiles of HI isolates from Chinese children and to provide guidelines for clinical treatment.
Methods: Our Infectious Disease Surveillance of Pediatrics (ISPED) collaboration group includes six children's hospitals in different regions of China. The same protocols and guidelines were used by all collaborators for the culture and identification of HI. The Kirby-Bauer method was used to test antibiotic susceptibility, and a cefinase disc was used to detect β-lactamase activity.
Results: We isolated 2073 HI strains in 2016: 83.9% from the respiratory tract, 11.1% from vaginal secretions, and 0.5% from blood. Patients with respiratory isolates were significantly younger than nonrespiratory patients (P < 0.001). Of all 2073 strains, 50.3% were positive for β-lactamase and 58.1% were resistant to ampicillin; 9.3% were β-lactamase-negative and ampicillin-resistant. The resistance rates of the HI isolates to trimethoprim-sulfamethoxazole, azithromycin, cefuroxime, ampicillin-sulbactam, cefotaxime, and meropenem were 71.1%, 32.0%, 31.2%, 17.6%, 5.9%, and 0.2%, respectively.
Conclusions: More than half of the HI strains isolated from Chinese children were resistant to ampicillin, primarily due to the production of β-lactamase. Cefotaxime and other third-generation cephalosporins could be the first choice for the treatment of ampicillin-resistant HI infections.
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