Author: Brian Holtry

Cholera is a disease of antiquity and probably represents some of the diarrheal illnesses described by Hippocrates and other early physicians. Robert Koch discovered V cholerae in 1884. Since the 17th century, at least eight epidemics of cholera have swept the globe. At least seven of the eight pandemics originated from the Ganges River delta, where cholera is endemic.

C fetus infection may manifest as fever, chills, and myalgias, without definitive localization; additionally, this organism displays a propensity to infect vascular structures. Endocarditis, intravascular infection of abdominal aortic aneurysms, and septic thrombophlebitis with vessel necrosis have been reported. Fetal death, even with appropriate antibiotic therapy, may occur. Fetal complications most commonly occur during the second trimester of pregnancy.

Campylobacter species are intestinal commensals in many animals, including cattle, pigs, sheep, chickens, and turkeys. Contamination of foodstuffs during meat and dairy processing is thought to significantly contribute to the spread of disease. Unpasteurized dairy products, undercooked meats, and contaminated water serve as the vehicles for Campylobacter and other bacterial pathogens.

Patients with septicemia, wound infections, or ear infections caused by a Vibrio species frequently have a history of shellfish ingestion or saltwater exposure. Clinical manifestations vary depending on the site of infection.

Noncholera gastroenteritis is often associated with recent ingestion of raw or undercooked shellfish and often occurs in the summer or early fall in the United States. A typical presentation includes explosive diarrhea, low-grade fever and chills, and mild-to-moderate abdominal pain with cramping.

Cholera is a fulminant diarrheal disease caused by V cholerae (Box 1). Patients with cholera develop frequent, watery stools, which may reach volumes =1 L/h.

Before 1990, strains of Haemophilus influenzae type b were found in the upper respiratory tract of 3-5% of children and a small percentage of adults. Colonization rates with type-b strains are even lower now, reflecting routine immunization of infants against H influenzae type b. Non-type-b encapsulated H influenzae are present in the nasopharynx of < 2% of individuals, whereas nonencapsulated (nontypable [see below]) strains colonize the respiratory tract of 40-80% of children and adults.

B catarrhalis causes bronchitis and pneumonia in patients with underlying lung disease, especially chronic obstructive pulmonary disease. It is also a rare cause of invasive disease, including meningitis, endocarditis, bacteremia without a focus, septic arthritis, and cellulitis.

The catarrhal stage is characterized by nonspecific upper respiratory symptoms, including rhinorrhea, mild cough, and low-grade fever. During this stage, which typically lasts 1-2 weeks, the disease is highly communicable. The paroxysmal stage is marked by sudden attacks or paroxysms of severe, repetitive coughing, often culminating with the characteristic whoop and frequently followed by vomiting.

H influenzae was first isolated during the 1892 influenza pandemic and was originally believed to be the causative agent of influenza. Although subsequent studies revealed the fallacy of this idea, H influenzae has proved to be a common cause of localized respiratory tract and systemic disease, including meningitis, epiglottitis, pneumonia, pyogenic arthritis, cellulitis, otitis media, and sinusitis, among others (Box 1). Meningitis is the most common and serious form of invasive H influenzae type-b disease. In the mid-1980s, before the introduction of effective vaccines, ~ 10,000-12,000 cases of H influenzae type-b meningitis occurred in the United States each year, and 95% of cases involved children < 5 years old.