Dysentery :: transmission
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Transmission due to contaminated hands is one of the important routes by which diarrhoea pathogens spread. The hands commonly become contaminated while cleaning the anus after defaecation. This study deals with the commonly used methods of anal cleansing in a low socioeconomic community in Rangoon, Burma and with the degree of hand contamination that results according to the method used. A cross-sectional survey was employed for collection of behavioural and hand contamination data. The incidence of acute diarrhoea and dysentery among under-fives in this community was monitored for 1 month and was correlated with the cleaning method used by their mothers. Water was the principal method used for cleaning the anus in all age groups. No one used toilet paper and only 4 to 9% used paper other than toilet paper. The level of education seemed to be a factor in determining the use of paper or water. The hands of mothers using water were more contaminated than those using paper. However, thorough hand washing with soap and water was found to be effective in decontaminating the hands. Furthermore, there was a relation between the incidence of diarrhoea and dysentery and the method of cleaning.
The role of the microbial flora of the large intestine in experimental Trichuris suis infection was studied by comparing the clinical syndrome in conventionally reared (CR) pigs, specific pathogen-free pigs, and gnotobiotic pigs. Thedisease in CR pigs was characterized by a severe mucohemorrhagic enteritis; in contrast, a mild catarrhal enteritis was observed in specific pathogen-free and gnotobiotic pigs. Spirochaetes and vibrio-like organisms were observed only in CR pigs and increased during the clinical phase of the disease. The clinical syndrome was not transmitted by oral administration of intestinal or fecal material from infected CR pigs to CR pigs free of T. suis. Smaller numbers of T. suis produced diarrhea in CR pigs and significantly reduced the growth rates of infected animals; clinical signs and the reduction in growth rate was prevented by incorporating an antibacterial substance (dimetridazole) in the food. Although clinical trichuriasis closely resembles swin dysentery, the two syndromes seem to be distinct. The present results suggest that a microbial component acts synergistically with T. suis to produce the severe clinical syndrome in CR pigs, but identification of the microbial component and the mechanism by which clinical signs are produced await further studies of the bacterial flora of the large intestine of pigs.
Fecal shedding of Treponema hyodysenteriae, transmission of disease, and humoral antibody production against the large spirochete were evaluated in pigs convalescent from experimentally induced swine dysentery. Untreated pigs (n = 21) and 5 pigs that had been treated with virginiamycin were included in the study. Treponema organisms were culturally detected in the feces of 2 untreated pigs as long as 70 and 71 days, and in the feces of 1 treated pig as long as 83 days after the last clinical evidence of disease. Of 8 convalescent pigs that intermittently discharged T hyodysenteriae in their feces, 4 transmitted clinical disease to exposed susceptible pigs. One of the convalescent animals has been free of clinical signs of disease for 57 days before introduction of the susceptible pigs. Treated and untreated convalescent pigs developed similarly elevated agglutinin titers that were maintained as long as 150 days after infection. There was no apparent correlation between the frequency or duration of fecal shedding of the spirochetes and the magnitude of the agglutinin titers of the convalescent pigs.
Swine dysentery (SD) was transmitted to healthy pigs by contact with experimentally-induced carrier pigs. Carrier pigs were produced by exposure of specific pathogen-free (SPF) swine to swine acutely affected with SD. When carrier pigs became acutely affected with SD, they were allowed to recover naturally or were treated with dimetridazole or ronidazole. Recovery was based on disappearance of clinical signs of SD. At a given time after recovery, normal SPF swine were housed with the carriers in a disinfected isolation unit to determine the ability of carriers to transmit SD. In each of 3 experiments, carriers that had recovered and remained asymptomatic for 11 to 25 days transmitted SD to contacts in 14 to 51 days. In 2 experiments, pathogenic Treponema hyodysenteriae was isolated from carriers 12 days before clinical SD was observed in contacts. Carriers which had recovered and remained asymptomatic for 70 and 90 days transmitted SD to contacts in 1 of 3 experiments. Treponema hyodysenteriae was isolated only from contacts with clinical signs of SD. In 4 experiments, carriers that had been treated with nitroimidazole compounds and subsequently recovered for 19 to 44 days failed to transmit SD. Culture of fecal samples on trypticase soy agar with 5% bovine blood and 400 microgram of spectinomycin/ml was helpful in predicting the carrier state, but phase contact contact microscopy of wet fecal smears was not.
The therapeutic effects of 2 dose levels of lincomycin and a reference drug (tylosin) were compared in 80 growing pigs with experimentally transmitted swine dysentery (SD). The pigs were allotted equally to 4 groups. Treatment was initiated 5 days after pigs were exposed to SD. Lincomycin was administered IM at doses of 11.0 or 4.4 mg/kg of body weight once daily for 3 to 7 days. Tylosin was injected IM at a dose of 8.8 mg/kg once daily for 3 days (highest recommended dose). The control (nontreated) infected pigs were not given the drug. The effects was terminated 22 days after exposure to SD. The effects were measured in terms of mortality, survival, physical activity, performance, and necroscopy findings. The 2 drugs reduced the clinical signs of SD. Pigs treated with either dose of lincomycin had a better treatment response than did pigs treated with tylosin, as evidenced by less mortality, longer survival time, and greater feed intake (P = 0.05). In addition, pigs treated with the larger dose of lincomycin, 11.0 mg/kg, had better treatment responses in 12 of the 14 measured criteria than did pigs treated with tylosin. Also, these pigs treated with the larger lincomycin dose had better treatment responses tha did the pigs treated wih the smaller dose of lincomycin, 4.4 mg/kg, as evidenced by dysentery, fecal consistency, physically active and intermediately active pig days, body weight gain, and feed intake.
Of 25 outbreaks of swine dysentery investigated, 22 were considered to have resulted from the purchase of pigs from farms known to be infected, two from the introduction of Treponema hyodysenteriae on the boots of the stockman, and one from the accidental entry of infected pigs into a 'closed' herd. The hidden costs of swine dysentery in terms of an increased food conversion ratio may be more than four times the cost of medication. A method of halting the spread of disease is described.