Brucella canis is a Gram-negativebacterium in the family Brucellaceae that causes brucellosis in dogs and other canids. It is a non-motile short-rod or coccus-shaped organism, and is oxidase, catalase, and urease positive.[1]B. canis causes infertility in both male and female dogs. It can also cause inflammation in the eyes. The hosts of B. canis ranges from domestic animals to foxes and coyotes.[2] It is passed from species to species via genital fluids. Treatments such as spaying, neutering, and long-term antibiotics have been used to combat B. canis. The species was first described in the United States in 1966 where mass abortions of beagles were documented.[3]Brucella canis can be found in both pets and wild animals and lasts the lifespan of the animal it has affected.[2]B. canis has two distinct circular chromosomes that can attribute to horizontal gene transfer.[4]
Brucella are non-motile meaning that they cannot move themselves and they must have assistance. This is because B. canis does not have flagella. Brucella are also non-encapsulated, non-spore forming bacteria that replicate in the ER of their host cells.[5] Cells typically measure ~0.5-0.7 x 0.6-1.5 µm and occur slightly, in pairs, or short chains.[6]They are Gram-negative and have a coccobacilli (short rod) shape. They have slightly rounded ends, with slightly outward curving sides.[7] On blood or chocolate agar, colonies are small (~0.5-2 mm after 48-72 hours), convex, non-hemolytic and non-pigmented. Often B. Canis colonies can present themselves as rough variants.[8] The optimal growth temperature for B. canis is 37°C, but growth is still possible within the range from 20°C to 40°C. Additionally, the pH range in which B. canis grows most effectively is from pH 6.6 - 7.4, making this organism neutrophilic in nature.[7]
Brucella have an unusual composition of fatty acids that make up their outer cell membrane. Myristic, palmitic, and stearic acids are all found in large quantities within the outer cell membrane. Cis-vaccenic and arachidonic acids are found in medium amounts, while C17 and C19 cyclopropane fatty acids are found in very limited amounts. Additionally, there are no hydroxy fatty acids present in Brucella outer cell membranes. This particular composition of fatty acids is believed to be the reason behind hydrophobic interactions that occur within the outer cell membrane and lead to greater cell stability.[7] Importantly, B. Canis is a "natural rough" Brucella. Its Lipopolysaccharide lacks the O-polysaccharide that is present in smooth strains; an envelope trait that influences colony phenotype and host interaction without implying a-virulence.[9]
B. canis is also unique from other Brucella species in that the lipids that make up its phospholipid portion are mainly cis-vaccenic cyclopropane with small amounts of lactobaccilic acid. This differs from other Brucella species, as they demonstrate the opposite composition, with lactobacillic acid making up the majority of the phospholipid fraction. Brucella is unusual in this composition because lactobacillic acid is typically within Gram-positive organisms but not common within Gram-negative organisms such as Brucella.[7]These specific envelope features are discussed alongside the organisms hallmark intracellular cycle. After uptake, Brucella replicate within ER-derived Brucella containing vacuoles, a niche specific to replication and survival within B. Canis.[10]
Identification
B. canis is a zoonotic organism. The bacteria are oxidase, catalase and urease positive and non-motile. Unlike haemophilus, which they resemble, they have no requirements for added X (hemin) and V (nicotinamide adenine dinucleotide) factors in cultures. Full identification is established by serology and PCR. Due to B. canis being naturally rough (lacking O-polysaccharide), smooth-antigen serology is unreliable. Modern practice uses B. canis-adapated serological assays such as RSAT/2-ME, IFAT and ELISA to make full identification.[11]B. canis is not acid-fast, but they tend to maintain their color when exposed to weak acids. This results in their red color when stained using Macchiavello's stain.[7] When isolated, B. canis is always in a rough form, with hydrophobic LPS imbedded in its outer membrane. MALDI-TOF mass spectrometry with validated databases and whole-genome sequencing (WGS) are now increasingly used for definitive confirmation of B. Canis and specific outbreak tracing.[12]
Colonies of Brucella can typically start to be seen after 48 hours. These colonies tend to be 0.5-1.0 mm in diameter, with a convex shape and are typically circular. Growth is often slower than other bacteria, with colonies requiring up to 72 hours for clear visualization.[13]B. canis presents itself as a rough species, so colonies are generally non-mucoid rather than sticky, glue-like of presenting smooth strains. Recent reports describe colonies as small, white to yellow-ish white and non-pigmented, consistent with rough Brucella.[14]
Metabolism
B. canis functions as a chemoorganotroph, deriving energy from the oxidation of organic compounds and utilizing organic electron sources. Studies indicate that B. canis, like other Brucella species, shares a conserved metabolic architecture within the genus. This includes a lack of 6-phosphofructokinase (PFK), an enzyme required for the Embden–Meyerhof–Parnas (EMP) pathway (classical glycolysis). Instead, glucose catabolism is accomplished using the pentose phosphate pathway.[15]B. canis utilizes oxygen as well as nitrate as its terminal electron acceptor within its electron transport chain. This electron transport system is known to function using cytochromes, and B. canis has the ability to utilize nitrate as a terminal electron acceptor due to the organism's ability to produce nitrate reductase.[7]
While some Brucella species require supplemental CO2 for growth, B. canis does not. B. canis has demonstrated growth on media containing thionine, but no growth on media containing basic fuchsin.[7]
Genome
B. canis has two distinct circular chromosomes. Chromosome 1 has 2,199 genes, and Chromosome 2 has 1,224 genes. These two circular chromosomes contain multiple distinct shared regions, which can be attributed to horizontal gene transfer.[4] Evidence suggests that Chromosome 2 was derived from a plasmid, though both chromosomes contain essential genes.[16]
B. canis is thought to be a variant of B. suis Biovar 1, based on the genomic similarities between the two. The genomic structure of both B. canis and B. suis Biovar 1, cannot be distinguished from each other as they both demonstrate similar sizes within the two circular chromosomes present. Based on this similarity B. canis is thought to be a stable R mutant of B. suis Biovar 1.[7]
Image of B. canis colonies growing on blood agar culture media.
Pathogenicity
The disease is characterized by epididymitis and orchitis in male dogs, endometritis, placentitis, and abortions in females, and often presents as infertility in both sexes. Other symptoms such as inflammation in the eyes and axial and appendicular skeleton; lymphadenopathy and splenomegaly, are less common.[17] Although there has been an increase in the international movement of dogs, Brucella canis is still very uncommon.[18] Signs of this disease are different in both genders of dogs; females that have B. canis infections face an abortion of their developed fetuses. Males face the chance of infertility, because they develop an antibody against their spermatozoa. This may be followed by inflammation of the testes which generally settles down a while after. Another symptom is the infection of the spinal plates or vertebrae, which is called diskospondylitis.[19] It is generally spotted in the animal's reproductive organs. This infection usually causes the animal to spontaneously abort a fetus and can also cause an animal to become sterile.[20]
Host range
The host range of the bacterium is mainly domestic dogs but evidence of infections in foxes and coyotes has been reported.[18]B. canis is a zoonotic organism[19] and although rare, humans can contract the infection. It is unlikely, but most common in dog breeders, those in laboratories dealing with the bacteria, or people who are immunocompromised.[21]
Transmission
B. canis is commonly transmitted via venereal routes, as well as physical contact with infected bodily fluids.[22]B. canis is passed through contact with fluids from the mucous membranes of the genitals (semen and vaginal discharge), eyes, and oronasal cavities. The highest bacterial loads of B. canis are found in the genital secretions of dogs infected with the bacteria.[22] Contact can occur during sexual activity as well as other daily grooming and social interactions. Though dog-to-dog transmission is most commonly during breeding, it can also happen after contact with uterine discharge, semen, and aborted material.[22]
High levels of B. canis exist in these secretions in the six weeks following abortion in females, and around six to eight weeks following infection in males. Lower levels of B. canis still remain in the semen of infected males for two years following infection, which can serve as a large source of transmission to other dogs.[18] Offspring of infected females can be infected with B. canis through intrauterine vertical transmission or via drinking the milk of the infected female.[22]
Urine can also serve as a route of transmission in males, as the bladder resides in close proximity to the prostate and epididymus. The bacterial load in the urine of infected dogs is lower than in genital discharges.[23] In their urine, infected dogs can carry up to 106 bacteria per milliliter, compared to the genital discharges that can carry up to 1010 bacteria per milliliter.[23] This leads to contamination of the urine making it another vehicle for B. canis transmission.[24] Infected dogs carry the highest bacterial load of B. canis after 1-6 months after infection.[23] Infected neutered animals are not able to display reproductive symptoms, however both intact and neutered dogs are able to shed B. canis in urine.[23] This means that both neutered and intact dogs are able to transmit the disease via urine.[23]B. canis is found to be localized in the prostate of male dogs, thus transmitting through the urine in both intact and neutered males.[23]
Treatment
Currently, there are not commercially available vaccines for B. canis.[25] Antimicrobial treatment and sterilization of the infected animals is considered an alternative to removing the animal.[25] There have been reports of anti-Brucella vaccines (used for cattle and small ruminants), used along with previously mentioned methods but is not considered practical due to its risk of vaccine strain shedding in a domestic environment with current vaccines maintaining an amount of virulence for humans.[25]
Treatment for B. canis is very difficult to find and often very expensive. The combination of minocycline and streptomycin is thought to be useful, but it is often unaffordable. Tetracycline can be a less expensive substitute for minocycline, but it also lowers the effect of the treatment.[26]
Long term antibiotics can be given but usually results in a relapse. Spaying and neutering can be effective, and frequent blood tests are recommended to monitor progress. Dogs in kennels that are affected by B. canis are usually euthanized for the protection of other dogs and the humans caring for them.[27]
B. canis is relatively easy to prevent in dogs. There is a simple blood test that can be done by a veterinarian. Any dog that will be used for breeding or has the capability to breed should be tested.
Ecology
Under natural conditions Brucella spp, including B. canis are obligate parasites and do not grow outside the host except in laboratory cultures. However, at specific temperatures and moisture levels Brucella can persist in soil and surface water up to 80 days. The bacterium can also survive for months in frozen conditions.[28]
B. canis is mainly found in dogs, but can also affect other wild canine species such as wolves, foxes, and coyotes.[29] The bacterium persists in these hosts, being an adaptive pathogen towards canines. The environment these hosts reside in further contribute to the canine specificity. Dog kennels are a favored environment for the bacterium to spread due to transmission through urine and reproductive fluids. It is also circulated through wildlife by hunting.[30]
History
B. canis was discovered by Leland Carmichael in 1966, when the bacterium was identified in canine vaginal discharge and the tissues from mass abortions in beagles.[18][31]B. canis was said to be a biovar of B. suis. With recent research, PCR assay data was able to contradict B. canis and B. suis. PCR data showed a complete difference between the two strains along with B. suis biovars unattained from B. canis DNA. PCR assays have been proven beneficial when differentiating between Brucella strains and vaccine strains.[32]
In the decades following its discovery, there has been an increase in infections caused by the bacterium due to the growing overseas adoption of dogs as pets.[33]
↑ Alton, G. G.; Forsyth, J. R. L. (1996), Baron, Samuel (ed.), "Brucella", Medical Microbiology (4thed.), Galveston (TX): University of Texas Medical Branch at Galveston, ISBN978-0-9631172-1-2, PMID21413351, retrieved 2025-09-25
↑ Brucellosis FAQs for Dog Owners. Georgia Division of Public Health in Partnership with the Georgia Department of Agriculture Office of the State Veterinarian, and the University of Georgia College of Veterinary Medicine, 13 June 2006, .
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