Camel tuberculosis–a case report

An adult male dromedary bull was diagnosed with pulmonary tuberculosis (Tb). The dromedary was severely emaciated and died 2 months after the onset of the disease. It exhibited typical Tb lesions in both lungs and lung lymph nodes. A guinea pig inoculated with lung tissue from the Tb camel died after 3 weeks from typical Tb. Mycobacteria were isolated from the dromedary's lung and lung lymph nodes and also from different organs of the guinea pig. The microorganism was identified as member of the antelope clade of the Mycobacterium tuberculosis complex.     

Two cases of equine grass sickness with evidence for soil-borne origin involving botulinum neurotoxin

Botulism is caused by different types of Clostridium botulinum, a soil bacterium. Equine grass sickness (equine dysautonomia) is suspected of being a clinical form of this disease. On a stud where this disease occurred twice within 8 months, grass and soil samples and necropsy specimens of one horse were tested for the presence of bacterial forms and toxin of C. botulinum. Different types and type mixtures (A-E) of C. botulinum and botulinum neurotoxin were found. For the first time, it has been shown that green grass blades contain botulinum toxin. The results support the hypothesis that equine grass sickness is a clinical form of botulism, a soil-borne disease.     

Seroepidemiologic studies of the detection of antibodies to Brucella, Chlamydia, Leptospira, BVD/MD virus, IBR/IPV virus and enzootic bovine leukosis virus (EBL) in dromedary mares (Camelus dromedarius)

Camels which are bred for the purpose of racing were tested serologically for 6 different animal diseases. The group were split into racing and breeding camels. The following results were achieved: Brucellosis, breeding camels 2%, racing camels 6.6%; Chlamydiosis 24%, 15%; Leptospirosis 2.5%, 5.6%; BVD/MD 9.2%, 3.6%. No antibodies were detected against IBR/IPV- and EBL-virus. The results are discussed under an epidemiological point of view.     

An attenuated herpes vaccine may protect Gyr hybrids from fatal inclusion body hepatitis. A preliminary report

Four Gyr hybrids were used for this falcon herpes vaccine experiment. Three falcons were given 1 ml of an attenuated falcon herpesvirus vaccine (DuFaHe) subcutaneously twice within 14 days, whereas the fourth falcon was used as a control. Eighteen days after the booster vaccination, all four Gyr hybrids were intranasally and ocularly challenged with a virulent low-passage falcon herpesvirus. The control falcon died 9 days after challenge with typical lesions of herpesvirus inclusion body hepatitis. The three vaccinated falcons seroconverted and did not show any symptoms. Following the challenge their antibody titres to falcon herpesvirus increased. No herpesvirus was isolated from any of the cloacal swabs taken during this experiment, indicating that there was no danger for any other birds from DuFaHe. This experiment shows that falcons can be protected from herpesvirus infection by an attenuated herpesvirus vaccine. However, it should be stressed that only four falcons were used for this experiment.     

Predisposing factors in enterotoxemias of camels (Camelus dromedarius) caused by Clostridium perfringens type A.

C. perfringens type A was isolated from different organs and intestines from breeding and racing camels which died from peracute and acute enterotoxemias in two separate outbreaks. Pathological changes in the digestive tract were mild in breeding camels, and severe in racing camels. A polyvalent clostridial antiserum of bovine origin given intravenously had a life-saving effect on breeding camels, but not on racing camels. In the two outbreaks, fifty percent of the breeding camels were suffering from an acute Trypanosoma evansi infection, and 25% of the racing camels had developed a salmonellosis. It is suggested that both infections played an important role as predisposing factors for the outbreak of C. perfringens enterotoxemias.     

Preliminary study of mucosal IgA in the equine small intestine: specific IgA in cases of acute grass sickness and controls

REASONS FOR PERFORMING STUDY: There is much evidence to suggest that group III Clostridium botulinum (types C and D) are involved in the aetiology of equine grass sickness (EGS). Antibodies have been detected previously in the blood and high levels associated with resistance to disease. Specific mucosal antibodies in the gastrointestinal (GI) tract are likely to be important in protection, and this study was performed to ascertain if such antibodies could be detected and if their levels were related to disease state. OBJECTIVES: To develop a method for quantifying IgA antibodies to C. botulinum types C and D in the GI tract of horses and to relate antibody levels to disease status. METHODS: Samples of tissue (n = 25: 6 duodenum, 7 jejunum and 12 ileum) were taken from acute grass sickness (AGS) cases and from control horses (n = 12; 4 samples from each site) at post mortem. They were extracted with the detergent saponin in the presence of protease inhibitors and assayed for total IgA, for specific IgA against botulinum neurotoxins types C and D (BoNT/C or BoNT/D), and against surface antigens of a BoNT/C negative strain of C. botulinum type C (SA) and of Clostridium tetani (TetSA), as a control. Specific IgA was expressed as percentage total IgA. RESULTS: Compared to controls, significantly higher levels of specific IgA against BoNT/C were detected in the jejunum (P = 0.04) and ileum (P = 0.02) of AGS cases. Similarly, higher specific levels against BoNT/D were demonstrated in duodenum (P = 0.01) and jejunum (P = 0.02). Significantly higher levels of IgA against SA were demonstrated only in duodenal samples (P = 0.01). CONCLUSIONS: Levels of IgA antibody to BoNTs in control horses were at near undetectable levels, suggesting no recent exposure to toxins. In AGS cases, significantly higher levels of specific IgA were detected predominantly in jejunum and ileum. POTENTIAL RELEVANCE: If specific IgA is protective then any successful vaccine for EGS should induce a mucosal response.