The novel coronavirus SARS-CoV-2 is a new member of the family Coronaviridae, genus Betacoronavirus, which was first described in a series of patients presenting with pneumonia in China. Similar to lessons learned from severe acute respiratory syndrome (SARS), although at a lower frequency, SARS-CoV-2 has tropism to the GI tract [3, 6]. The angiotensin-converting enzyme 2 (ACE2) receptor is believed to be responsible for the entrance of SARS-CoV-2 into the cells, and it is abundantly expressed in the GI tract epithelium. This may account for the GI symptoms of COVID-19 patients and the potential fecal–oral transmission of the disease [7, 8]. Indeed, there have been some pediatric cases with a confirmed diagnosis of COVID-19 who did not show respiratory symptoms as their initial and main presentations. They may initially be considered common pediatric illnesses other than COVID-19, such as febrile seizure or gastroenteritis, and lead to the spread of the disease in the community and among medical staff [9].
GI symptoms have been reported in children with COVID-19 either with or without respiratory symptoms. The most common GI symptoms were anorexia, vomiting, and diarrhea [2, 4, 10]. A few cases of GI bleeding have also been reported [2]. Although pediatric cases of COVID-19 with GI symptoms including abdominal pain and GI bleeding, and especially diarrhea, have been reported, the index case presented with dysentery with no clinical or radiological respiratory involvement, and to date, no similar case of dysentery as the only presentation in children with COVID-19 has been reported. Alternatively, different infectious etiologies might have caused dysentery and fever. However, no enteric bacterial pathogens or parasites other than SARS-CoV-2 were recovered from stool analysis and culture. The possibility of pseudomembranous colitis induced by the introduction of ceftriaxone was weak, as the patient had clinical and laboratory evidence of colitis prior to the administration of ceftriaxone.
Some physicians have attributed the GI symptoms to the hypoxia, as cell necrosis from tissue hypoxia may cause gastrointestinal mucosal cell damage, resulting in ulceration and hemorrhage [2]. However, our patient had no hypoxia and was not critically ill, and this may show that dysentery was the primary result of COVID-19 and that it can be considered as a new feature of this virus.
No respiratory symptoms were seen and the patient was not in critical condition; therefore, we did not use any antiviral treatment or hydroxychloroquine, as not only has the efficacy of these drugs on COVID-19 not yet been proven, but they may have significant adverse effects. We also followed the patient until both nasopharyngeal and stool tests were negative to determine the duration of viral shedding and the required isolation period. In many cases of COVID-19, viral shedding can continue beyond 14 days with positive RT-PCR tests; nevertheless, the follow-up of every patient for long periods of time in routine practice is not possible. On the other hand, the positive RT-PCR tests beyond the resolution of symptoms may not necessarily indicate the possibility of disease transmission, as in some cases of COVID-19, the high viral load at admission can account for this finding.
In conclusion, pediatric patients with COVID-19 usually do not present with typical clinical features of the infection, which is respiratory involvement. Dysentery may be the only presentation of this disease, and long-term isolation should be considered, as the viral shedding may last for more than a month. We aimed to increase awareness among pediatricians and other clinicians in considering COVID-19 as a possible etiology for abdominal pain and dysentery in children.
