Campylobacter fetus involves in multiple threat. It triggers intestinal illness and systemic infections. Those at higher risk are the elderly humans with weak immunity, people occupationally exposed to infected ruminants like cattle and sheep.  

Most Campylobacter infections result in diarrhea. The 0.15% of cases progress to a bloodstream infection, with C. fetus with a small percentage of these cases. The incidence rate for blood culture confirmed bacteremia with 53%. It is found in cattle, and sheep as the primary reservoirs for C. fetus. With DNA detection in 2.4% of intestinal campylobacteriosis cases and the mortality rate is about 14%. 

A retrospective study from Limoges Teaching Hospital provided data on 20 patients (15 males), with an average age of 73, who had C. fetus infections primarily associated with hematologic and neoplasms diseases. Blood cultures diagnosed 17 patients, with 20% of isolates resistant to amoxicillin and 30% to fluoroquinolones. Epidemiological links for 9 humans infected with this subspecies suggest potential associations with Asian foods or reptile exposure. 

Campylobacter fetus is gram-negative pathogen, it belongs to group called Campylobacteraceae. The bacterium needs oxygen to live.  

They bear rod shaped morphology with S-shape resembling spirochaete. The cells appear as mono cells and in short chains. Sometimes, they are in pairs. 

Arabinogalactan that is resistant to acid staining, is the primary composition of its cell wall. They are. Some Campylobacter fetus obtain flagella for movement.  

Other features like pili or hair-like threads appears externally for surfaces sticking. The cells of Campylobacter have different shapes. 

Campylobacter fetus surface layer is called the Capsule or S Protein. The layer covers the bacteria in a crystal pattern.  

One subspecies, C. fetus venerealis is sharing 92% of the same genes for this S-layer protein.  

C. fetus makes lipases and hemolysins which damage cells and increase inflammation during infections. The type strain is ATCC 27374.

C. fetus venerealis has a larger genome containing a chromosomal element called ICE84112 that acts like a plasmid to transfer genes laterally. 

Campylobacter human infection remain unclear. Some routes are by forming biofilms and shielding against immunity and drugs. C. fetus produces proteases that damage host tissues allowing them to spread in the body. 

The intestinal Campylobacter infection becomes invasive. Then the bacteria enter the bloodstream to cause bacteremia. This invasive form spreads to organs causing a systemic infection. Symptoms depend on the organ caused. C. fetus cause lung abscesses, and infections transmitted from mother to newborn. 

C. fetus infections lead to vascular issues like inflamed blood vessels, aneurysms, or inflammation of the heart lining. C. fetus resides in the intestines, potentially entering the bloodstream from there. Most gut Campylobacter infections don’t significantly disrupt the intestines.

Campylobacter fetus evade the body’s immune defenses by resisting destruction by serum & engulfment by immune cells due to a protective protein layer known as the S-layer. The layer develops crystal patterns to shield bacterial surfaces. The systemic circulation and preventing harmful substances and Campylobacter species. 

Immune cells engulf and kill Campylobacter by generating reactive oxygen species and nitric oxide. The complement system also helps. It coats C. fetus to make it easier for cells to eat it. Or it can burst the bacteria by forming a membrane attack complex. 

Campylobacter infections are characterized by catheter bacteremia precede soil exposure and can lead to systemic complications. Other associated clinical urinary infections, and endocarditis. 

Gut infections lead to Campylobacter in the blood and spreads illness elsewhere. Though most such gut issues come from C. jejuni or C. coli, some stem from C. fetus. Campylobacter causes lung abscesses and pregnancy issues. C. fetus causes infections reaching the bloodstream. 

While acute diarrhea presents the symptom of intestinal campylobacteriosis with Campylobacter fetus, the microbe can migrate, infecting distant body sites also. 

The routine method involves culturing the bacteria. This identifies C. fetus in infected animals or people. Campylobacter fetus is isolated from blood, and peritoneal fluid using bacteriological methods. Culturing on media yields white and convex colonies. 

Cefoperazone deoxycholate agar or blood agar is used as standard media. C. fetus grows as grey moist colonies within 40-48 hours when incubated at 25-37°C under microaerophilic conditions. 

Polymerase Chain Reaction assays quickly and precisely detect C. fetus genetic material. 

Clinical signs and microscopy using dark-field or phase contrast show curved, S-shaped, or spiral rods. These rods move rapidly and dart around in abomasal smears. 

Immunosorbent Assays identify specific antibodies against C. fetus and also recent or past infections. 

Educating the public and healthcare experts may help the control of infection. 

In healthcare settings implementing infection control practices is more imperative to prevent the spread of L. goodfellowii. 

Adherence to hand hygiene protocols and disinfection of medical devices with continuous surveillance of antibiotic resistance patterns. 

Campylobacter fetus bloodstream infection: risk factors and clinical features – PubMed (nih.gov) 

Campylobacter Fetus – an overview | ScienceDirect Topics