Shigella

Shigellosis, a common intestinal infectious disease caused by Shigella bacteria, is also known as Bacillary dysentery, often referred to simply as "Bacillary dysentery." This bacterium is a major intestinal pathogen in humans and primates, while other animals are generally less susceptible. Clinically, it manifests with sudden onset, chills, high fever, abdominal pain, diarrhea, and the passage of pus- or blood-streaked stools, often accompanied by tenesmus. Given the current scarcity of monkey resources, there is an increasing likelihood of encountering monkeys from unidentified sources. Moreover, Shigella bacteria exhibit high susceptibility within monkey populations. Therefore, monitoring for Shigella is particularly critical.

Shigella is a non-motile, Gram-negative enteric pathogen that causes bacterial dysentery or shigellosis. It lacks a capsule and does not form spores, making it a facultative anaerobe—though it thrives best under aerobic conditions. When cultured on standard media for 24 hours, Shigella forms convex, circular colonies with neat edges, measuring approximately 2 mm in diameter and exhibiting transparency. Shigella is divided into four major subspecies: Flexneri (Group B), Dysenteriae (Group A), Boydii (Group C), and Sonnei (Group D). Based on the structure of their O-antigen lipopolysaccharides, these subspecies are further classified into multiple serotypes: Flexneri includes 14 serotypes, Dysenteriae has 15, Boydii encompasses 20, and Sonnei consists of just 1 serotype.

Shigella distribution is influenced by economic development. Flexneri Shigella is predominantly found in developing countries, accounting for 60% of cases, while Sonnei Shigella has a higher isolation rate in developed countries and regions. Boydii Shigella, meanwhile, remains largely confined to Bangladesh and Southeast Asia. Together, Flexneri and Sonnei Shigella account for the vast majority of Shigella cases—65.9% and 23.7%, respectively.

The natural hosts of Shigella bacteria are humans and primates. Shigellosis is highly contagious, with as few as 10 to 100 bacteria sufficient to cause infection. Outbreaks often occur during summer, spreading primarily through the fecal-oral route—either directly from person to person or indirectly via ingestion of water or food contaminated by the feces of infected individuals. Shigellosis is a severe disease in young primates, particularly those that have never been exposed before. Young primates encountering asymptomatic carriers for the first time may become infected. Infant monkeys can also harbor Shigella bacteria; under conditions of immune suppression, they may develop clinical shigellosis. Both scenarios could explain the high incidence of clinical shigellosis observed when young primates are introduced into new social groups. During these transitions, added stressors such as changes in living environments may increase the animals' susceptibility to the disease or trigger clinical symptoms in previously asymptomatic carriers. Chronic subclinical carriage of Shigella has already been documented in both humans and non-human primates.

The incubation period for Shigella typically ranges from 12 to 48 hours, though it may sometimes take up to a week. Symptoms generally vary from mild to severe infections. In monkeys, the main clinical manifestations include acute typical bacillary dysentery, acute atypical bacillary dysentery, acute exacerbation of chronic bacillary dysentery, and chronic sluggish-type dysentery. Pathological changes often reveal hemorrhagic colitis or purulent-hemorrhagic colitis in the cecum and colon, or alternatively, acute catarrhal enteritis with occasional ulcers and bleeding. Shigella bacteria are capable of penetrating the mucosal layer, replicating within epithelial cells, and spreading between cells. Infected cells eventually undergo apoptosis, leading to patchy defects in the mucosa. Ulcerative colitis is the underlying cause of watery, mucoid diarrhea, and fecal samples from infected individuals often contain abundant neutrophils and red blood cells. Biopsy specimens from areas affected by Shigella infection typically exhibit edema, accompanied by capillary congestion, focal hemorrhages, crypt hyperplasia, depletion of goblet cells, infiltration of both mononuclear and polymorphonuclear (PMN) cells, shedding of epithelial cells and red blood cells, as well as micro-ulcers.

Shigella bacteria invade the colonic and rectal epithelium of primates and humans, triggering the acute mucosal inflammation characteristic of shigellosis. Infection typically remains confined to the superficial layers of the colonic mucosa, but severe tissue damage can lead to abscesses and ulcers. Disruption of the epithelial layer results in clinical symptoms such as watery diarrhea, intense abdominal pain, and cramping—eventually progressing to the bloody, mucus-like stools that hallmark bacillary dysentery. Without effective treatment, patients with shigellosis may develop secondary complications, including sepsis, pneumonia, and hemolytic uremic syndrome, underscoring the importance of ongoing research in this area.

Antibiotics can be used to treat shigellosis, reducing the duration of bacterial excretion in patients. However, Shigella flexneri is increasingly developing antibiotic resistance, with resistance to commonly used, more affordable antibiotics on the rise—placing additional strain on limited healthcare services in developing countries.

Effective antibiotic treatment can reduce the average duration of the illness from about 5 to 7 days down to 3 days, while also shortening the period of pathogen shedding. When the isolated strain is susceptible, orally administered drugs such as ampicillin (2 grams daily for 5 consecutive days) may be effective. Trimethoprim (8 mg/kg/day) and sulfamethoxazole (40 mg/kg/day) rapidly eliminate susceptible microorganisms in the gut; however, Shigella bacteria are increasingly developing resistance to these medications. In contrast, ciprofloxacin (1 gram daily for 3 days) remains effective against many drug-resistant strains.

If animals at the experimental monkey breeding facility become infected, targeted and timely medication can be administered to the entire group based on the results of antimicrobial susceptibility tests. At the same time, enhanced measures should be taken to improve farm hygiene and implement rigorous disinfection protocols—specifically, thoroughly cleaning and flushing the enclosures twice daily. Additionally, more than two effective disinfectants with varying concentrations should be used in rotation to spray and disinfect enclosure floors, walls, and hanging rings. For comprehensive coverage, space fumigation disinfection can also be applied. By combining medical treatment with meticulous environmental sanitation and disinfection, we can prevent the spread of infection, thereby avoiding unnecessary economic losses.

References

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