Seroepidemiology of Q fever in one-humped camel population in northeast Iran.

Coxiella burnetii, an obligate intracellular bacterium, is the causative agent of important zoonotic Q fever. It is the etiological agent of coxiellosis or Q fever in animals and human. This seroepidemiological survey was conducted to determine the seroprevalence of coxiellosis in increasingly camel raised population in vast area of Khorasan (North, South, and Razavi) provinces, northeast Iran. Using cluster random sampling strategy, 167 camels in 11 counties were selected as serum samples. Sera were assayed for antibody against C. burnetii using a Q fever ELISA kit. Logistic regression model was used to insight the contributing risk factor(s) of Q fever in the study area. C. burnetii was widely distributed throughout the study area. Seroprevalence of C. burnetii at animal level was 28.7 % [(95 % confidence interval (CI): 21.83, 35.56)] for camel populations. The proportion of seropositivity for camels in the studied counties ranged from 0 to 63.6 %. Logistic regression model showed that age correlated with seroprevalence of coxiellosis at the individual level in camels (P < 0.05). This study showed that a relatively high proportion of camels are seropositive to C. burnetii. Considering the economic, zoonotic, and public health importance of Q fever, percussion measures are to be implemented to prevent spreading of C. burnetii and zeroing the risk of Q fever in farm animals and human in this agro-ecologically and geopolitically important region.

First identification of Mycoplasma capricolum subspecies capripneumoniae in goats in Iran.

Mycoplasma capricolum subspecies capripneumoniae (Mccp) is the etiological agent of caprine contagious pleuropneumonia (CCPP) disease. The CCPP is one of the most severe diseases of goats. A herd of 2,000 goats located in the countryside of Tehran city, Iran, was examined for the study in August 2021. In history taking, observation, inspection and clinical examination, high case fatality rate (46.00%) due to respiratory distress and high morbidity of pleuropneumonia (15.00%) syndrome were recorded. Accordingly, ten carcasses of goats were dissected. The epidemiological pattern of the disease, clinical examination findings and the signs of necropsy of dead patients were suspected to CCPP. Four lung samples of necropsied goats were sent to the laboratory for PCR test and in all of them, Mccp was detected and CCPP was also confirmed. The disease was controlled by two measures: (a) the whole herd was first treated with antibiotics (florfenicol and tylosin) and (b) then the Pulmovac-In vaccine was then administered. This study is the first documented report of CCPP occurrence caused by Mccp in Iran and shows the importance of availability of effective vaccines to control and prevention of CCPP.

Subchronic neurotoxicity of diazinon in albino mice: Impact of oxidative stress, AChE activity, and gene expression disturbances in the cerebral cortex and hippocampus on mood, spatial learning, and memory function.

Diazinon (DZN) with prominent neurotoxic effects perturbs CNS function via multiple mechanisms. This investigation intends to explore mood, spatial learning, and memory dysfunction, acetylcholine esterase (AChE) activity, and neurodegeneration-related gene expression in the cortex and hippocampus regions of mice exposed to DZN for 63 consecutive days (subchronic exposure). Adult male albino mice were orally given sublethal DZN (DZNL = 0.1 mg/kg, DZNM = 1 mg/kg and DZNH = 10 mg/kg). All mice in the DZNH group died within 3 weeks postexposure. DZNL and DZNM caused body and brain weight loss (p < 0.05). Completing 9 weeks of DZN exposure, a marked decline in AChE activity and oxidative stress level was indicated in both brain regions (p < 0.05). Also, synaptophysin, vesicular acetylcholine transferase, and glutamate decarboxylase gene expressions were affected in both brain regions (p < 0.05). Furthermore, the present study revealed that DZN administration increased anxiety and depressive-like behaviors (p < 0.0001). Spatial learning and short- and long-memory were severely affected by DZNL and DZNM treatments (p < 0.0001). Taken together, subchronic exposure to low and medium doses of DZN can cause AChE inhibition, oxidative damage, and neurotransmitter disturbances in brain cells and induce neurodegeneration. These changes would impair mood, spatial learning, and memory function.