The epidemiology of Phytobacter ursingii is not well understood, as this species was only recently described in 2018. However, some studies have reported the occurrence and characteristics of Phytobacter ursingii infections in humans, mainly in the United States and Brazil. Here are some of the main findings: 

• Phytobacter ursingii is a rare cause of bacteremia (bloodstream infection) in humans, accounting for less than 1% of all Enterobacterales bacteremia cases. 
• Phytobacter ursingii bacteremia is mainly associated with underlying conditions such as diabetes, cancer, or immunosuppression and presents with symptoms such as fever, chills, hypotension, and septic shock. 
• Phytobacter ursingii bacteremia has a high mortality rate, ranging from 25% to 50% in different studies. 
• Phytobacter ursingii can be challenging to identify by conventional biochemical tests, as it shares many characteristics with other Enterobacterales species, especially Pantoea agglomerans. Molecular methods, such as 16S rRNA gene sequencing or Mass spectrometry using matrix-assisted laser desorption ionization time-of-flight (MALDI-TOF), can provide more accurate identification. 
• Phytobacter ursingii can also pose a challenge for antimicrobial therapy, as it can carry genes that confer resistance to extended-spectrum β-lactams and carbapenems, which are usually mediated by genetic mobile elements. Moreover, Phytobacter ursingii can protect co-infecting sensitive bacteria from the action of antibiotics by producing enzymes that degrade or modify the drugs. Therefore, susceptibility testing and combination therapy are recommended for treating Phytobacter ursingii infections. 

• Kingdom: Bacteria 
• Phylum: Pseudomonadota 
• Class: Gammaproteobacteria 
• Order: Enterobacterales 
• Family: Enterobacteriaceae 
• Genus: Phytobacter 
• Species: P. ursingii 

The structure of Phytobacter ursingii is a topic of interest for microbiologists and clinicians, as this species is a rare and emerging pathogen that can cause severe infections in humans.

Based on the web search results, here are some points about the structure of Phytobacter ursingii: 

• Phytobacter ursingii is a Gram-negative bacterium, which means that it has a thin layer of peptidoglycan in its cell wall and is stained pink by the Gram stain method. 
• Phytobacter ursingii is rod-shaped, with a cell length of 0.9-1.2 micrometers and a cell width of 0.6-0.7 micrometers. 
• Phytobacter ursingii is motile, with amphitrichous flagella, which are hair-like structures that extend from both ends of the cell and help it move in liquid environments. 
• Phytobacter ursingii is non-pigmented, which means that it does not produce any visible color on the culture media. 
• Phytobacter ursingii is non-encapsulated, which means that it does not have a polysaccharide layer outside its cell wall that protects it from the host immune system. 

• Phytobacter ursingii was identified in 2018 from three clinical strains that were isolated from human sputum in South Carolina, USA, in 1974. These strains were previously classified as Brenner’s Biotype XII of the Erwinia herbicola-Enterobacter agglomerans-Complex. 
• Phytobacter ursingii can be differentiated from Phytobacter diazotrophicus, the type species of the genus, by its ability to metabolize d-serine and l-sorbose. However, there is no information available on the antigenic types of Phytobacter ursingii, which are the variants of a microorganism that differ in their surface antigens and can elicit different immune responses.
• Antigenic typing is usually based on serological methods, such as agglutination tests or enzyme-linked immunosorbent tests (ELISA), which identify specific antibodies directed against the microorganism’s antigens. Phytobacter ursingii antigenic types of identification, further studies are needed to isolate and characterize its surface antigens and test their reactivity with different antisera.

The pathogenesis of Phytobacter ursingii in humans needs to be better understood, as this species was only recently described in 2018. However, based on the available literature, some possible mechanisms of infection and disease are: 

• Phytobacter ursingii can enter the human body through contaminated medical devices or fluids, such as catheters or total parenteral nutrition. The bacteria can then colonize the bloodstream and cause bacteremia, which is a severe condition where bacteria enter the bloodstream and cause inflammation and organ damage. 
• Phytobacter ursingii can evade the host immune system by producing enzymes that degrade or modify antibiotics, such as extended-spectrum β-lactamases and carbapenemases. These enzymes can also protect co-infecting sensitive bacteria from the action of antibiotics, creating a synergistic effect. 
• Phytobacter ursingii can cause tissue damage and inflammation by releasing endotoxins, which are lipopolysaccharides (LPS) that are a component of the Gram-negative bacteria’s outer membrane. Cytokines can be released in response to endotoxins and additional agents of inflammation, which may result in septic shock, a life-threatening complication that causes multiple organ failure and death. 

Phytobacter ursingii can cause opportunistic infections in humans, particularly in individuals with indwelling catheters or those who are immunocompromised or have total parenteral nutrition. It can also produce extended-spectrum β-lactamase and carbapenem-resistance genes, which make it resistant to many antibiotics. Therefore, host defenses of Phytobacter ursingii are essential to prevent or control the infection. 

Some of the host defenses of Phytobacter ursingii are: 

• Innate immunity: This is the first line of defense against microbial invaders. It is made up of external barriers like skin and mucous membranes and cellular and molecular components, such as phagocytes, natural killer cells, complement systems, and cytokines. Innate immunity can recognize and eliminate Phytobacter ursingii by various mechanisms, such as opsonization, phagocytosis, oxidative burst, and inflammation. 
• Adaptive immunity: This is the second line of defense that is specific, diverse, and memory-based. It consists of two types of lymphocytes: B cells and T cells. Antibodies produced by B cells are able to attach to the antigens of Phytobacter ursingii and neutralize them or mark them for destruction by other immune cells. T lymphocytes can eradicate diseased cells directly or stimulate other immune cells by secreting cytokines. Adaptive immunity can also generate memory cells that can provide long-term protection against Phytobacter ursingii. 
• Colonization-resistance: This is the ability of the normal microbiota of the human body to prevent the colonization and growth of pathogenic bacteria, such as Phytobacter ursingii. The normal microbiota can compete with Phytobacter ursingii for nutrients, space, and receptors or produce antimicrobial substances, such as bacteriocins, that can inhibit its growth. Colonization resistance can also modulate the host immune system and enhance its response against Phytobacter ursingii. 

The symptoms of Phytobacter ursingii infection in humans are mainly related to bacteremia, which is a severe condition where bacteria enter the bloodstream and cause inflammation and organ damage. Some of the common symptoms of bacteremia are: 

• Fever and chills 
• Low blood pressure (hypotension) 
• Rapid heart rate (tachycardia) 
• Confusion or altered mental status. 
• Shortness of breath (dyspnea) 
• Nausea and vomiting 
• Abdominal pain 
• Skin rash or lesions 

The degree of the illness will determine how these symptoms change, the presence of other underlying diseases, and the response of the immune system. 

• Diagnosing Phytobacter ursingii infection can be challenging due to its rarity and similarity to other Enterobacterales species, particularly Pantoea agglomerans. Conventional biochemical tests may not be accurate.
• Molecular methods like 16S rRNA gene sequencing or MALDI-TOF mass spectrometry are recommended for precise identification. Unique features include the ability to metabolize d-serine and l-sorbose and the production of indole. Performing a blood culture test is crucial, as Phytobacter ursingii is primarily associated with bacteremia in humans. Blood culture confirms the presence and quantity of bacteria, aiding in severity assessment and guiding antibiotic therapy through susceptibility testing. 

The prevention of Phytobacter ursingii infection in humans is mainly based on avoiding exposure to the bacteria and maintaining good hygiene practices. Some of the possible ways to prevent Phytobacter ursingii infection are: 

• Avoid contact with contaminated medical devices or fluids, such as catheters or total parenteral nutrition, which can be sources of Phytobacter ursingii entry into the human body. If you need to use these devices or fluids, make sure they are sterile and adequately handled by trained healthcare workers. 

• Use soap and water to wash your hands thoroughly and often, especially before and after touching wounds, catheters, or other medical devices. It can help prevent the transmission of Phytobacter ursingii and other bacteria from your hands to your body or other people. 
• Disinfect surfaces and equipment that may be contaminated with Phytobacter ursingii or other bacteria, such as countertops, sinks, faucets, toilets, and medical instruments. Use appropriate disinfectants and follow the manufacturer’s instructions. 

• (anonymous) (dsmz.de) 
• A retrospective study of the incidence, clinical characteristics, identification, and antimicrobial susceptibility of bacteremic isolates of Acinetobacter ursingii | BMC Infectious Diseases | Full Text (biomedcentral.com)