Look What the Cat Dragged in! Recurrent Clostridioides difficile from a Household Cat.

A 31-year-old woman presented with a 1-week history of fever and diarrhea. She reported passing 4 loose, non-bloody bowel movements daily, associated with abdominal cramps, nausea, and vomiting. Medical history included endometriosis and recurrent urinary tract infections (UTIs). Her most recent UTI was treated with a 7-day course of ciprofloxacin, completed 3 days prior to admission. This was her only antibiotic exposure within the previous 3 months. She denied any previous hospitalizations, surgeries, prior CDI, other enteric infections, or family history of immune-mediated conditions or IBD. Pertinent negatives were dysuria, melena, or hematochezia. She did not smoke or drank alcohol socially, and had only 1 male sexual partner. On physical examination, she was febrile (38.89°C), tachycardic (133 beats/min), and tachypneic (respiratory rate 22 breaths/min), but normotensive. There was minimal abdominal tenderness and no guarding. The white blood cell count was 13 950 cells/μL, lactic acid 2.8 mg/dL, and urinalysis revealed trace leukocyte esterase. The urine culture was negative, but she received 2 days of intravenous antibiotics for a suspected urinary tract infection (UTI). Computed tomography of her abdomen and pelvis with contrast suggested left pyelonephritis; the colon was normal. The stool polymerase chain reaction (PCR) was positive for C. difficile, and she was discharged home with oral vancomycin for 14 days. She reported resolution of her diarrhea after completion of the 14-day course. As demonstrated in Figure 2 , 2 months later, she presented to a primary care clinic with recurrence of her symptoms, including profuse watery diarrhea associated with abdominal pain, nausea, fever, and chills. Her stool PCR was again positive for C. difficile . She had not used any other antibiotics between the initial episode and recurrence of CDI. She was given a regimen of tapered and pulsed vancomycin. A month later, via video visit, she revealed that she continued to have profuse diarrhea, every 4 hours, and fidaxomicin was prescribed. It was during this visit that the patient asked if a stray cat she adopted approximately a month before the onset of her initial symptoms might have contributed to her condition. She had plans at this time to isolate herself from her cat and take her cat to the veterinarian for testing while completing her fidaxomicin course. Given chronic diarrhea, she was referred to gastroenterology for further evaluation. One month later, the cat stool antigen test was positive for C. difficile , and treatment was commenced by a veterinarian. The cat displayed no symptoms; however, the patient was also concerned about the cat’s health, given the proximity to her in her apartment and the temporal relationship of the symptom onset and her adoption of the pet. One month later, she saw her gastroenterology doctor who had previously found her stool to be positive (by PCR) for the C. difficile toxin gene. She began treatment with bezlotoxumab. The patient described that the symptoms were not resolved until both her and her cat were treated. The patient followed up in clinic 2 months later without any gastrointestinal complaints and confirmed resolution of symptoms.

The increasing incidence of community-associated Clostridioides difficile infections (CA-CDI) has implicated natural reservoirs from animals such as domestic cats and dogs, livestock, shell-fish, and wild animals [ 1 ]. Understanding the interactions between the human host, the host’s environment, and the infectious agent is the key to this case ( Figure 1 ). Recurrent Clostridioides difficile infection (CDI) from a household cat represents a novel presentation of CA-CDI, which, by definition, refers to CDI in an individual with no overnight stay in an inpatient healthcare facility in the 12 weeks prior to symptom onset [ 2 , 3 ].

Environmental factors play a significant role in the pathogenesis of recurrent community-acquired CDI. A study in Houston, Texas identified pathogenic C. difficile in household and public environments; recovering toxigenic C. difficile endospores in 32% of samples collected from various household items and community areas, compared with 16.5% positive isolates from hospitals [ 4 , 5 ]. The most common sources were parks (24.6% samples positive), followed by homes (17.1%), commercial stores (8.1%), and fast-food restaurants (6.5%). There is a general lack of data on the prevalence of pathogens in household pets and on the incidence of human infections that can be attributed to pets [ 6 ]. However, it has been hypothesized before that a patient who experiences CDI could transmit C. difficile to a pet, and the pet could then act as a reservoir for recurrence of C. difficile in the original patient or colonization of those who did not carry the pathogen [ 7 ]. There is yet to be a study that demonstrates the direct transmission of C. difficile between household pets and their owners, but Loo et al found that 2/9 (22%) of cats and 2/5 (40%) of dogs belonging to owners that had experienced CDI carried identical strains of C. difficile [ 8 ]. Studies have shown isolates of pathogenic clones of C. difficile in cat feces; specifically, the RT 014 strain [ 1 , 4 ]. However, there is no evidence that this bacterium is pathogenic to cats. Furthermore, evidence from stool-sample isolation that humans and their pets had similar strains of C. difficile makes it possible that our patient’s recurrent CA-CDI was derived from this natural reservoir [ 1 ]. It is also worth noting that although the rates of recurrent CDI in cats are not well known, it is hypothetically possible that the cat mentioned in our case could become re-infected and cause a recurrent infection in the patient. Given these findings, both household and environmental reservoirs must be considered in the etiology of CA-CDI. This study was limited by the fact that whole genome sequencing was not performed on stool isolates. As such, resolution of the patient’s stool microbiota was limited. Additionally, the patient was exposed to ciprofloxacin prior to her initial CDI which is a risk factor for CDI.

In conclusion, given the temporal relationship between the patient’s symptom onset and the adoption of the cat, and given the resolution of the patient’s symptoms following treatment of the cat, it is possible that the patient acquired C. difficile from the cat. This case highlights the importance of comprehensive history taking and considers the zoonotic transmission of C. difficile as a novel etiology of CA-CDI.