It’s hard to resist those big, pleading eyes in the pet store window. But buyer beware. Pet store puppies may infect people with a bacteria for which no common antibiotic treatment exists, a new study warns.
Campylobacter jejuni (C jejuni) cannot be treated with any common antibiotics and is an increasing public health threat, according to researchers at the U.S. Centers for Disease Control and Prevention, who investigated 168 cases of C jejuni infection linked to pet store puppies.
“These outbreaks indicate that pet store puppies are a source of extensively drug-resistant C jejuni infections in the United States,” said researcher Dr. Mark Laughlin. He’s an epidemic intelligence service officer in the CDC’s Division of Foodborne, Waterborne and Environmental Diseases.
“Data indicate these extensively drug-resistant C jejuni strains have been circulating for at least 10 years, and no sources other than dogs have been identified,” Laughlin said.
Beginning in the summer of 2011, the CDC started seeing an increasing number of C jejuni cases among people who had contact with pet store puppies.
Of the cases investigated by the CDC, 137 happened in January 2016 through February 2020, and 31 others dated to 2011. Overall, 97% of the patients said they had contact with a dog in the week before getting sick, and 88% said they had contact with a pet store puppy. Of all the cases, 88% were from highly drug-resistant C jejuni.
These infections were not from any particular breeder, transporter, distributor, store or chain, the researchers noted.
C jejuni can spread among puppies in crowded environments, since transmission typically occurs through infected food or water or contact with infected feces, Laughlin said.
Pets, including cats and dogs, can carry C jejuni and other germs that can make you sick, he said.
“That’s why it’s important to think about your and your family’s health when you are getting or caring for a pet,” Laughlin said. “When choosing a puppy or dog, pick one that is bright, alert and playful.”
Signs of illness in pets include appearing sluggish or tired, not eating, diarrhea and breathing abnormally. Even a dog that appears healthy, however, can spread germs to people and other animals, Laughlin said.
“If your dog becomes sick soon after purchase or adoption, take your dog to a veterinarian right away,” he advised. “If you recently purchased or adopted your dog, tell the pet store, breeder or rescue organization about the pet’s illness.”
To curb the spread of this bacteria, Laughlin said the commercial dog industry should take action to stop the spread of C jejuni from pet store puppies to people.
Laughlin also noted that it’s not clear if these infections are also found in shelters.
“We don’t know if dogs adopted from shelters are safer,” he said. “We do know that during the study period, we did not see evidence of this strain being passed from dogs adopted from shelters.”
The CDC also recommends that pet store workers practice proper hand hygiene, eat and store food properly, clean up messes safely, follow store protocols for identifying and reporting sick or injured animals, and practice responsible use of antibiotics for the animals in their stores.
According to Dr. Teresa Murray Amato, head of emergency medicine at Northwell Health Long Island Jewish Forest Hills in New York City, “Campylobacter jejuni is the most common cause of diarrheal disease in the United States.”
Most people recover within roughly a week after their first symptoms and don’t need any intervention, she said.
“Some people, however, are more vulnerable, such as the elderly, the very young and people with underlying conditions, and require antibiotics to treat the disease,” Amato added.
The last few years have seen an emergence of drug-resistant C jejuni, including strains for which there are no effective antibiotic treatments today, Amato said.
“In patients with diarrheal illness that does not respond to antibiotics, doctors should ask if the patient has been in contact with a puppy within seven days from onset of symptoms,” she said. “If you or a loved one is concerned about exposure, please contact your doctor to review your risk factors.”
In the United States, Campylobacter causes an estimated 1.5 million illnesses and 450,000 antibiotic-resistant infections each year, according to the CDC.
The most common cause of bacterial gastroenteritis worldwide is the foodborne zoonotic bacterium Campylobacter jejuni (C. jejuni). C. jejuni is an intestinal commensal in a variety of animals (particularly in poultry), but after fecal–oral transmission is pathogenic in the human intestine, causing an acute infective colitis.
Campylobacteriosis is characterized by watery, bloody diarrhea, abdominal cramps, fever, and intestinal inflammation [1].
The infection is usually self-limiting and only symptomatic treatment is required, but chronic progression or infections in immunocompromised patients require antibiotic treatment. A proportion of campylobacteriosis patients develop sequelae such as Guillain–Barré syndrome, reactive arthritis, or irritable bowel syndrome (IBS).
Studies in C. jejuni-infected volunteers indicated that an acute inflammatory response is a hallmark of the infection [1]. Experimental studies revealed a strong interrelation between the mucosal immune response and epithelial barrier dysfunction in C. jejuni infection: the ‘leaky gut’ phenomenon [2,3,4].
The pre-hormone vitamin D (VD) regulates innate and adaptive immune responses. Its precursor cholecalciferol (calciol; (3β,5Z,7E)-9,10-secocholesta-5,7,10(19)-trien-3-ol) is metabolized to the intermediate calcidiol (25-hydroxycholecalciferol) and then to biologically active vitamin D3 (calcitriol; 1,25-dihydroxycholecalciferol).
Low serum VD levels increase susceptibility to acute and chronic illnesses such as infectious diseases, IBS, inflammatory bowel disease (IBD), and colorectal cancer [5,6,7,8]. VD is well known for its role in bone metabolism, but is also involved in regulating the absorptive and immune functions of the gastrointestinal tract [9].
In the intestine, vitamin D is required for cell differentiation, proliferation, and for the maintenance of epithelial barrier function, in addition to its effects on calcium and phosphate transport [10].
The biological active form of VD is hydroxylated to calcitriol by 1-α-hydroxylase (also known as cytochrome P450 enzyme CYP27B1) and regulates further target genes in a complex with the VD receptor (VDR) and the retinoid X receptor (RXR). Evidence for the barrier-strengthening potential of VD has come from studies in IBD [11].
VD also exhibited barrier-protective and anti-inflammatory properties in in vitro and in vivo studies, but without a clear explanation for its molecular mechanism of action [12,13,14,15,16,17]. Nevertheless, clinical studies have shown a beneficial effect of VD treatment on diarrhea in IBD patients [18], which raises the possibility that it might also improve bacteria-induced diarrhea.
In this regard, VD supplementation increased the viability of intestinal epithelial cells, and partially restored the reduced transepithelial electrical resistance (TER) that occurred during C. jejuni infection [2]. Furthermore, in a preclinical intervention mouse study, VD decreased the inflammatory response that occurred during campylobacteriosis [14].
In the present study, we built on our previous work using bioinformatics to identify the relevance of the VD pathway in campylobacteriosis [2] by investigating (i) whether C. jejuni-induced barrier dysfunction can be treated or prevented by VD supplementation, and (ii) how C. jejuni interferes with the VD pathway.
reference link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8396270/
More information: The U.S. Centers for Disease Control and Prevention has more about Campylobacter jejuni.
