Glaesserella parasuis
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| Glaesserella parasuis | |
|---|---|
Scientific classification  | |
| Domain: | Bacteria |
| Kingdom: | Pseudomonadati |
| Phylum: | Pseudomonadota |
| Class: | Gammaproteobacteria |
| Order: | Pasteurellales |
| Family: | Pasteurellaceae |
| Genus: | Glaesserella |
| Species: | G. parasuis |
| Binomial name | |
| Glaesserella parasuis (Biberstein & White 1969) Dickerman et al. 2020[1] | |
| Synonyms | |
|
Haemophilus parasuis Biberstein & White 1969 | |
Glaesserella parasuis (formerly known as Haemophilus parasuis) is a Gram-negative bacterium belonging to the family Pasteurellaceae. It is best known as the causative agent of Glässer's disease in pigs.
Originally described as Haemophilus parasuis by Biberstein and White in 1969, it was reclassified into the newly created genus Glaesserella in 2020 based on comprehensive phylogenomic analyses.[1]
Morphology
Glaesserella parasuis is a Gram-negative coccobacillus. Cells typically appear as short rods or coccobacilli, often forming pairs or short chains. It is non-motile and non-spore-forming.[2]
Growth conditions
The bacterium requires enriched media containing NAD (V factor) and exhibits optimal growth under aerobic conditions at 37 °C. Colonies typically appear small, smooth, and translucent on chocolate agar or blood agar supplemented with NAD.[2]
Clinical significance
Glaesserella parasuis is the causative agent of Glässer's disease, an infectious condition characterized by polyserositis (inflammation of serosal surfaces), arthritis, meningitis, and pneumonia, primarily affecting young piglets.[3]
Epidemiology
The bacterium commonly colonizes the upper respiratory tract of pigs, and outbreaks of disease typically occur when piglets are under stress or have compromised immunity, such as during weaning.[4]
Clinical signs
Affected animals may exhibit fever, respiratory distress, lameness, joint swelling, and neurological symptoms. Mortality rates can be significant without appropriate treatment or preventive measures.[3]
Diagnosis
Diagnosis involves clinical observations, necropsy findings (such as fibrinous polyserositis), and laboratory confirmation through bacterial isolation and molecular techniques such as PCR.[5]