What is your diagnosis? Spherical gas opacity indicating emphysematous cholecystitis.
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OBJECTIVE: To compare the frequency of isolation, genotypes, and in vivo production of major lethal toxins of Clostridium perfringens in adult dairy cows affected with hemorrhagic bowel syndrome (HBS) versus left-displaced abomasum (LDA). DESIGN: Case-control study. ANIMALS: 10 adult dairy cattle with HBS (cases) and 10 adult dairy cattle with LDA matched with cases by herd of origin (controls). PROCEDURE: Samples of gastrointestinal contents were obtained from multiple sites during surgery or necropsy examination. Each sample underwent testing for anaerobic bacteria by use of 3 culture methods. The genotype of isolates of C. perfringens was determined via multiplex polymerase chain reaction assay. Major lethal toxins were detected by use of an ELISA. Data were analyzed with multivariable logistic regression and chi2 analysis. RESULTS: C. perfringens type A and type A with the beta2 gene (A + beta2) were the only genotypes isolated. Isolation of C. perfringens type A and type A + beta2 was 6.56 and 3.3 times as likely, respectively, to occur in samples from cattle with HBS than in cattle with LDA. Alpha toxin was detected in 7 of 36 samples from cases and in 0 of 32 samples from controls. Beta2 toxin was detected in 9 of 36 samples from cases and 0 of 36 samples from controls. CONCLUSIONS AND CLINICAL RELEVANCE: C. perfringens type A and type A + beta2 can be isolated from the gastrointestinal tract with significantly greater odds in cattle with HBS than in herdmates with LDA. Alpha and beta2 toxins were detected in samples from cows with HBS but not from cows with LDA.
Experiments were conducted to determine the efficacy in stimulating and maintaining an immune response in the presence of maternal antibodies, compare the extent of the anamnestic responses to revaccination, and compare the maternal antibody response of 2- or 5-mL clostridial vaccination. In Exp. 1, 118 nursing calves were randomly assigned to receive a 2-mL (Alpha-7, A7) or a 5-mL clostridial vaccine (Ultrabac 7; UB7) at 50.4 +/- 15.30 (X +/- SD) d of age (d 0 = date of calving). Calves were revaccinated with the same treatment on d 170. Blood samples were collected from 10 calves of each treatment group on d 50, 170, and 191 to determine antitoxin units for Clostridium perfringens type C (PC) and D (PD) and agglutination titers for Cl. chauvoei (CC). The A7-treated calves tended (P < .10) to have higher PC units on d 170, an increased rate of change in PD units from d 170 to d 191 (P < .06), and a tendency (P < .10) for enhanced CC titers on d 191 compared with UB7-treated calves. In Exp. 2, 109 pregnant cows and 83 pregnant heifers were randomly assigned within a 2 x 2 x 2 factorial design. The main effects were dam age (cow or heifer), dam treatment (A7 or UB7), and calf treatment (A7 or UB7). Dams were vaccinated with A7 or UB7 d 124 prepartum (d -124) and d 53 after birth. At d 53.4 +/- 12.88, calves were vaccinated with A7 or UB7 (d 53). Calves were revaccinated with the same treatment on d 173. Blood samples were collected from 10 dams per treatment group on d -124, 53, and 173 and from their calves on d 53, 173, and 194. Cows had higher antitoxin levels for PC (P < .01) and PD (P < .05) than heifers. The A7-treated dams had higher (P < .01) PD units on d 53 and d 173 and CC on d 173 than did UB7-treated dams. Calves from A7-treated cows had higher (P < .03) PD units on d 53 than calves from UB7-treated cows. The A7-treated calves had higher titers for CC (P < .01) on d 173 than did UB7-treated calves, and this enhanced level seemed to continue to d 194 (P < .08). In conclusion, titers for clostridial diseases in 50- to 53-d-old calves can be enhanced if dams are vaccinated approximately 4 mo before calving, and 120 d between clostridial vaccinations seems to be too long for adequate protection.
Faecal samples from adult horses and from foals with diarrhoea or with normal faeces were evaluated for the presence of Clostridium difficile, C. difficile toxins, C. perfringens enterotoxin (CPE) and C. perfringens spore counts. Clostridium difficile was isolated from 7/55 horses (12.7%) and 11/31 foals (35.5%) with colitis, but from 1/255 normal adults (0.4%) and 0/47 normal foals (P<0.001). Clostridium difficile toxins A and/or B were detected in 12/55 diarrhoeic adults (21.8%) and 5/30 diarrhoeic foals (16.7%) but in only 1/83 adults (1.2%) and 0/21 foals with normal faeces (P<0.001 and P<0.05, respectively). Clostridium perfringens enterotoxin was detected in 9/47 diarrhoeic adults (19%) and 8/28 diarrhoeic foals (28.6%), but was not detected in 47 adult horses (P<0.002) or 4 foals (P = 0.22) with normal faeces. The positive predictive value of isolation of C. perfringens with respect to the presence of CPE was only 60% in adult horses and 64% in foals. There was no association between total C. perfringens spore count and CPE in the faeces. The overall mortality rate from colitis was 22% for adult horses and 18% for foals. Clostridium difficile toxin-positive adult horses with colitis were less likely to survive than C. difficile-negative horses with colitis (P = 0.03). This study provides further evidence that C. difficile and enterotoxigenic C. perfringens are associated with equine enterocolitis.
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Massive hemolysis with acute renal failure occurred in a previously healthy 69-year-old patient as a complication of Clostridium perfringens septicemia secondary to gall bladder empyema. To our knowledge, this is one of the few patients with C. perfringens septicemia and massive intravascular hemolysis who survived the episode and regained a normal renal function.
A dose response study was conducted to determine the appropriate (optimal) lincomycin concentration in drinking water for the treatment of necrotic enteritis (NE) in broilers. The study was replicated twice over time using a total of 2,895 broilers. Birds were raised in a facility containing a built-up litter from a source that experienced NE. They were commingled from 1 day of age until NE was observed. Lincomycin was mixed in drinking water at a rate of 0, .528, 2.114, 8.454, or 33.818 mg/liter for a period of 7 days. The study was terminated 3 weeks after initiation of therapy. Necrotic enteritis was diagnosed by mortality and pathological findings. The data on mortality were analyzed statistically using analysis of variance procedures. The Walker-Carmer technique was applied to estimate the appropriate lincomycin concentration. Lincomycin was effective for the treatment of NE in broilers at concentrations of greater than or equal to 2.114 mg/liter of drinking water. The minimal effective dose that would achieve maximal treatment response (optimal dose) against NE in broilers was estimated to be 16.9 mg lincomycin/liter of drinking water.
The efficacy of 16.9 mg lincomycin/liter of drinking water was evaluated for the treatment of necrotic enteritis (NE) in 743 broiler-type chickens. Birds were raised in a facility containing a built-up litter obtained from a source that experienced NE. They were commingled from 1 day of age until NE was observed. Two groups of 6 pens each were given 0 or 16.9 mg lincomycin/liter of drinking water. Water medication was offered fresh daily for 7 days and the study was terminated 3 weeks after initiation of therapy. The susceptibility of Clostridium perfringens to lincomycin was determined in vitro. The test organism was susceptible to lincomycin as reflected by minimal inhibitory concentration and minimal lethal concentration of .156 microgram/ml. Mortality attributed to NE was 0% in lincomycin treated birds and 14% in nonmedicated control birds (P less than .01). Lincomycin water medication was highly effective for the treatment of NE in broilers.
In an experiment to determine methods of incorporating soft winter wheat into broiler diets, a significant increase in mortality was observed in broilers fed wheat in crumbled diets. This increase in mortality was associated with necrotic enteritis with Clostridium perfringens indicated as the causative pathogen and complicated by a coccidiosis outbreak. When yellow corn was used in the diet, mortality was 2.9%. Use of all wheat, ground with a hammer mill, increased mortality to 28.9%. However, roller mill-ground wheat diet resulted in a mortality of 18.1%. When the grain component was approximately 50% wheat and 50% corn, mortality was 12.6% for broilers fed hammer mill-ground wheat and 3.4% for roller mill-ground wheat. Grain and feed were tested for several mycotoxins. Low levels of deoxynivalenol were found in both corn and wheat diets, but no differences between the corn and wheat-based diets were found that would explain the incidence of enteritis.
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Newborn conjunctival cultures were obtained from 35 babies prior to silver nitrate application and 48 hours later. On initial culture, 46 facultative bacteria and 27 anaerobes were recovered; 48 facultative and 18 anaerobes were recovered after 48 hours. Haemophilus vaginalis, Bacteroides species and anaerobic cocci decreased in numbers, whereas S. epidermidis, Micrococcus and Propionibacterium acnes increased during this time interval. Clostridial species were isolated from two cases who developed conjunctivitis, along with Peptostreptococcus in one of the cases. In vitro experiments demonstrated lack of killing of C. perfringens in silver nitrate concentrations of 0.1 percent, even after 24 hours exposure.
The prevalence of the enterotoxin gene in a well-characterized collection of 71 Clostridium perfringens strains from 36 separate food-poisoning cases or outbreaks was analyzed with the polymerase chain reaction (PCR). The clonality of 39 strains originating from 14 outbreaks where at least two isolates were available was studied with pulsed-field gel electrophoresis (PFGE) using SmaI and ApaI restriction endonucleases. The cpe gene PCR assay was found to correlate well with Clostridium perfringens enterotoxin (CPE) production in vitro with reverse passive latex agglutination. Of the C. perfringens food and clinical food-poisoning isolates 24 (86%) and 38 (88%) were cpe-positive, respectively. Different PFGE patterns indicated that multiple cpe-positive clones are frequently present within one outbreak. The existence of cpe-positive and negative isolates with identical or nearly identical PFGE patterns in a single outbreak suggests that the cpe gene may be in a movable genetic element.
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OBJECTIVE: To report a case of enteritis necroticans acquired in Australia, and to review the history, epidemiology, pathogenesis, clinical features, management and prevention of this disease. CLINICAL FEATURES: A 44-year-old diabetic and alcoholic restaurateur of Chinese-Malay origin, who had been living in Australia for over 20 years, was admitted to hospital with bloody diarrhoea which progressed to fulminant toxaemia and circulatory collapse, and ultimately required laparotomy. Typical pathological features and the isolation of Clostridium perfringens type C from faeces confirmed the diagnosis of enteritis necroticans. INTERVENTION AND OUTCOME: He was treated initially with ampicillin, gentamicin, metronidazole and chloramphenicol, and later with penicillin and metronidazole, and he required large volumes of intravenously administered fluid and blood for his toxaemic, hypotensive state. Laparotomy was performed as a life-saving procedure. Despite a lengthy convalescence, the patient recovered. CONCLUSIONS: Enteritis necroticans is a rare disease in developed countries, however it is likely to be underdiagnosed. Clinicians are encouraged to be on the alert for signs of severity that may indicate the need for laparotomy in a predisposed individual with features of this condition.
A previously healthy captive female bottlenosed dolphin (Tursiops truncatus) died suddenly. At necropsy, Clostridium perfringens was isolated from dorsal muscle, blood, left heart ventricle, thoracic fluid, and abdominal fluid. An identical strain was recovered from pool water. A male dolphin in the same pool had inflicted several "rake" marks on the dorsal surface of the female. Water-borne bacteria probably entered these lesions which served as the focus for anaerobe penetration and spread.