Salmonella is a genus of bacteria responsible for salmonellosis, a common foodborne illness that affects millions of people globally each year. This infection is acquired through the consumption of contaminated food or water. The illness is largely characterized by acute gastroenteritis, though the bacterial action involves a sequence of survival, invasion, and immune manipulation. Understanding this process reveals how this microbe can cause illness ranging from a self-limiting digestive upset to a severe, life-threatening systemic infection.
The Journey Through the Digestive System
The infection begins when Salmonella bacteria are ingested, requiring them to first survive the hostile environment of the upper digestive tract. The highly acidic conditions of the stomach, with a pH below 3, naturally destroy most microbes. However, Salmonella has evolved adaptive mechanisms that grant it a degree of acid tolerance, allowing a subset of the bacteria to survive this initial defense.
The surviving bacteria move into the small intestine, where they must contend with bile salts, a different type of antimicrobial defense. The bacteria possess regulatory systems that mediate resistance to bile, enabling them to establish themselves and multiply in the intestinal lumen. Once sufficient numbers are present, the bacteria migrate toward the intestinal lining, primarily targeting the lower small intestine and the colon. They use specialized surface structures, such as fimbriae, to attach to the epithelial cells and M cells, which are part of the gut-associated lymphoid tissue.
Triggering Acute Gastrointestinal Illness
The core of the acute illness starts when the Salmonella bacteria actively invade the cells lining the small and large intestines. They utilize a specialized needle-like structure called a Type III secretion system (T3SS) to inject bacterial proteins directly into the host cell. This injection manipulates the host cell’s internal structure, causing the cell membrane to ruffle and effectively engulf the bacteria in a process known as bacterial-mediated endocytosis.
Once inside, the bacteria reside within a protective bubble called the Salmonella-containing vacuole, where they continue to replicate. The invasion and damage to the epithelial cells trigger a massive inflammatory response. Localized inflammation is intensified by the release of pro-inflammatory messengers, such as cytokines, from the infected cells.
This inflammatory reaction recruits immune cells, particularly neutrophils, to the site of infection in the gut lining. This inflammation disrupts fluid balance in the intestine. This disruption leads to the hallmark symptoms of salmonellosis, including the sudden onset of diarrhea, which may contain mucus or blood, and abdominal cramping. Fever, nausea, and vomiting are also common symptoms resulting from this systemic inflammatory state.
Spread Beyond the Intestines
While most non-typhoidal Salmonella infections remain localized to the gut, the bacteria can spread beyond the intestinal barrier. This systemic spread, known as bacteremia or septicemia, occurs in a small percentage of healthy individuals, but is a risk in vulnerable populations. Infants, the elderly, and those with compromised immune systems are at a heightened risk for this invasive disease.
To achieve systemic dissemination, Salmonella can be taken up by migratory immune cells, such as dendritic cells and macrophages, and then transported through the lymphatic system into the bloodstream. Once in the blood, the bacteria can circulate and establish secondary infections in distant organs and tissues. This can lead to serious complications, including infections of the meninges surrounding the brain and spinal cord, the lining of the heart, or the bones and bone marrow.
Immune Response and Bacterial Clearance
The host immune system mounts a response to clear the Salmonella infection, involving both innate and adaptive components. Innate immune cells, such as phagocytes and neutrophils, are quickly recruited and attempt to engulf and destroy the bacteria. The coordinated action of the adaptive immune system, specifically T-cells, plays a substantial role in resolving the infection by activating macrophages and promoting bacterial clearance.
For most people, the infection is self-limiting, with symptoms resolving within four to seven days. Even after symptoms disappear, bacterial shedding occurs, meaning the person continues to excrete Salmonella in their feces. Shedding can persist for several weeks; in rare instances, individuals may become chronic carriers, shedding the bacteria for a year or longer. This prolonged shedding is a public health concern because it allows the bacteria to transmit to new hosts, perpetuating the cycle of infection.