Chapter 122. Acute Infectious Diarrheal Diseases and Bacterial Food Poisoning (Part 4) doc

Acute Infectious Diarrheal Diseases and Bacterial Food Poisoning Part 4 Host Defenses Given the enormous number of microorganisms ingested with every meal, the normal host must combat

Chapter 122 Acute Infectious Diarrheal Diseases

and Bacterial Food Poisoning

(Part 4)

Host Defenses

Given the enormous number of microorganisms ingested with every meal, the normal host must combat a constant influx of potential enteric pathogens Studies of infections in patients with alterations in defense mechanisms have led to

a greater understanding of the variety of ways in which the normal host can protect itself against disease

Normal Flora

The large numbers of bacteria that normally inhabit the intestine act as an important host defense by preventing colonization by potential enteric pathogens Persons with fewer intestinal bacteria, such as infants who have not yet developed normal enteric colonization or patients receiving antibiotics, are at significantly greater risk of developing infections with enteric pathogens The composition of the intestinal flora is as important as the number of organisms present More than

99% of the normal colonic flora is made up of anaerobic bacteria, and the acidic

pH and volatile fatty acids produced by these organisms appear to be critical elements in resistance to colonization

Gastric Acid

The acidic pH of the stomach is an important barrier to enteric pathogens,

and an increased frequency of infections due to Salmonella, G lamblia, and a

variety of helminths has been reported among patients who have undergone gastric surgery or are achlorhydric for some other reason Neutralization of gastric acid with antacids or H2 blockers—a common practice in the management of hospitalized patients—similarly increases the risk of enteric colonization In addition, some microorganisms can survive the extreme acidity of the gastric environment; rotavirus, for example, is highly stable to acidity

Intestinal Motility

Normal peristalsis is the major mechanism for clearance of bacteria from the proximal small intestine When intestinal motility is impaired (e.g., by treatment with opiates or other antimotility drugs, anatomic abnormalities, or hypomotility states), the frequency of bacterial overgrowth and infection of the small bowel with enteric pathogens is increased Some patients whose treatment

for Shigella infection consists of diphenoxylate hydrochloride with atropine

(Lomotil) experience prolonged fever and shedding of organisms, while patients

treated with opiates for mild Salmonella gastroenteritis have a higher frequency of

bacteremia than those not treated with opiates

Immunity

Both cellular immune responses and antibody production play important roles in protection from enteric infections The wide spectrum of viral, bacterial, parasitic, and fungal gastrointestinal infections in patients with AIDS highlights the significance of cell-mediated immunity in protection from these pathogens Humoral immunity is also important and consists of systemic IgG and IgM as well

as secretory IgA The mucosal immune system may be the first line of defense against many gastrointestinal pathogens The binding of bacterial antigens to the luminal surface of M cells in the distal small bowel and the subsequent presentation of antigens to subepithelial lymphoid tissue lead to the proliferation

of sensitized lymphocytes These lymphocytes circulate and populate all of the mucosal tissues of the body as IgA-secreting plasma cells

Genetic Determinants

The mechanisms underlying genetic variation in host susceptibility remain poorly understood People with blood group O show increased susceptibility to cholera, shigellosis, and norovirus infection A polymorphism in the interleukin 8

gene is associated with increased risk of diarrhea from enteroaggregative E coli

Approach to the Patient: Infectious Diarrhea or Bacterial Food Poisoning

The approach to the patient with possible infectious diarrhea or bacterial food poisoning is shown in Fig 122-1

Figure 122-1

Clinical algorithm for the approach to patients with community-acquired infectious diarrhea or bacterial food poisoning Key to superscripts:

1 Diarrhea lasting >2 weeks is generally defined as chronic; in such cases, many

of the causes of acute diarrhea are much less likely, and a new spectrum of causes

needs to be considered 2 Fever often implies invasive disease, although fever and

diarrhea may also result from infection outside the gastrointestinal tract, as in

malaria 3 Stools that contain blood or mucus indicate ulceration of the large

bowel Bloody stools without fecal leukocytes should alert the laboratory to the possibility of infection with Shiga toxin–producing enterohemorrhagic

Escherichia coli Bulky white stools suggest a small-intestinal process that is

causing malabsorption Profuse "rice-water" stools suggest cholera or a similar

toxigenic process 4 Frequent stools over a given period can provide the first warning of impending dehydration 5 Abdominal pain may be most severe in

inflammatory processes like those due to Shigella, Campylobacter, and

necrotizing toxins Painful abdominal muscle cramps, caused by electrolyte loss, can develop in severe cases of cholera Bloating is common in giardiasis An

appendicitis-like syndrome should prompt a culture for Yersinia enterocolitica

with cold enrichment 6 Tenesmus (painful rectal spasms with a strong urge to

defecate but little passage of stool) may be a feature of cases with proctitis, as in

shigellosis or amebiasis 7 Vomiting implies an acute infection (e.g., a

toxin-mediated illness or food poisoning) but can also be prominent in a variety of

systemic illnesses (e.g., malaria) and in intestinal obstruction 8 Asking patients

whether anyone else they know is sick is a more efficient means of identifying a common source than is constructing a list of recently eaten foods If a common source seems likely, specific foods can be investigated See text for a discussion

of bacterial food poisoning 9 Current antibiotic therapy or a recent history of

treatment suggests Clostridium difficile diarrhea (Chap 123) Stop antibiotic treatment if possible and consider tests for C difficile toxins Antibiotic use may

increase the risk of other infections, such as salmonellosis 10 See text (and Chap

117) for a discussion of traveler's diarrhea (After Guerrant and Steiner; RL

Guerrant, DA Bobak: N Engl J Med 325:327, 1991; with permission.)