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Canine parvovirus (CPV) is a fast-evolving single-stranded DNA virus that causes severe and fatal gastrointestinal disease in dogs. Lately, several mutations affecting viral protein (VP) capsid resulting in highly pathogenic variants with distinctive immunological and clinicopathological characteristics abound. This study involved screening stools of 44 randomly selected clinical cases of canine gastroenteritis from 4 cities (Ibadan, Jos, Makurdi, and Zaria) in Nigeria for CPV antigen using an on-the-spot immunoassay test kit, as well as, molecular detection of viral nucleic acid by polymerase chain reaction. Subsequently, nucleic acid sequencing of 1195-bp amplicons encompassing the VP2 encoding region was done. The resultant 40 high-quality amino acid sequences obtained were analysed for the identification and grouping of the viruses into their discrete variants - CPV-2a, CPV-2b, or CPV-2c, using key amino acids substitutions - Asn, Asp, or Glu respectively at position 426 of the VP2 gene. One-third (11/40; 27.5%) of the analysed sequences were identified as CPV-2a and two-third (29/40; 72.5%) as CPV-2c. The original CPV and CPV-2b were not detected. Also, the "new CPV-2a variant" with mutation S297A identified had two additional mutations (Y324I and T440A) associated with selective pressure and vaccination failure in their sequences. Similarly, unique CPV-2c mutants carrying genetic markers (S297A, Y324I, and Q370R) that are highly related to CPVs of Asian origin were observed. These findings revealed a high level of divergence of existing CPVs in circulation; suggesting that CPV is rapidly evolving in Nigeria lately. • More CPV-2c than CPV-2a was detected in the clinical samples analysed. • The New CPV-2a variant containing mutation S297A identified had two additional mutations responsible for vaccination failure. • The analysed CPVs exhibit a high level of genetic divergence from previous ones. • The Nigerian CPV-2c mutants carry genetic markers that are highly related to CPVs of Asian origin. [ABSTRACT FROM AUTHOR]

• MPX has a good killing effect on A. pleuropneumoniae better than that of PR39. • MPX significantly reduces A. pleuropneumoniae biofilm formation. • MPX downregulates virulence gene expression of A. pleuropneumonia. • Sap A gene plays an important role in A. pleuropneumoniae resistance to MPX. • MPX significantly reduces lung damage induced by A. pleuropneumoniae infection in vivo. Actinobacillus pleuropneumoniae is the causative agent of highly contagious and fatal respiratory infections, causing substantial economic losses to the global pig industry. Due to increased antibiotic resistance, there is an urgent need to find new antibiotic alternatives for treating A. pleuropneumoniae infections. MPX is obtained from wasp venom and has a killing effect on various bacteria. This study found that MPX had a good killing effect on A. pleuropneumoniae and that the minimum inhibitory concentration (MIC) was 16 μg/mL. The bacterial density of A. pleuropneumoniae decreased 1000 times after MPX (1 × MIC) treatment for 1 h, and the antibacterial activity was not affected by pH or temperature. Fluorescence microscopy showed that MPX (1 × MIC) destroyed the bacterial cell membrane after treatment for 0.5 h, increasing membrane permeability and releasing bacterial proteins and Ca2+, Na+ and other cations. In addition, MPX (1 × MIC) treatment significantly reduced the formation of bacterial biofilms. Quantitative RT-PCR results showed that MPX treatment significantly upregulated the expression of the PurC virulence gene and downregulated that of ApxI, ApxII, and Apa1. In addition, the Sap A gene was found to play an important role in the tolerance of A. pleuropneumoniae to antimicrobial peptides. Therapeutic evaluation in a murine model showed that MPX protects mice from a lethal dose of A. pleuropneumoniae and relieves lung inflammation. This study reports the use of MPX to treat A. pleuropneumonia infections, laying the foundation for the development of new drugs for bacterial infections. [ABSTRACT FROM AUTHOR]