Vol. 21, No. 6
THE JOHNS HOPKINS MICROBIOLOGY NEWSLETTER
Tuesday, February 19, 2002
19 outbreaks were reported to DHMH during MMWR Week
7 (February 10 - February 16)
10 outbreaks of gastroenteritis:
*3 outbreaks in Montgomery Co. (1 in a nursing home,
1 in an assisted living facility, 1 in a school)
*2 outbreaks in Baltimore Co. (both in nursing homes
- 1 outbreak w/ 2 confirmed cases of S. sonnei)
*1 outbreak in Cecil Co. (nursing home)
*1 outbreak in Washington Co. (assisted living facility)
*1 outbreak in Charles Co. (nursing home)
*1 outbreak in Frederick Co. (nursing home)
*1 outbreak in Wicomico Co. (nursing home)
3 outbreaks of foodborne gastroenteritis (1 involving college students in St. Mary's Co, [exposure probably in Baltimore Co.]; 1 associated with a hotel in Montgomery Co.; 1 involving Prince George's Co. residents [exposure possibly at a restaurant in Charles Co.]).
3 outbreaks of influenza-like illness (1 at a retirement
home in Frederick Co.; 1 at a nursing home in Charles Co.; 1 at a nursing
home in Baltimore Co.)
1 outbreak of influenza-like illness/pneumonia at a nursing
home (Cecil Co.)
1 outbreak of influenza/pneumonia at a nursing home (Baltimore
City--confirmed Influenza B/2 chest X-ray positive pneumonias)
1 outbreak of influenza at a nursing home (Frederick
Co.)
The patient is a 3 year-old female without a significant past medical history who presented to The Johns Hopkins Emergency Department with 1 day history of diarrhea and fever of 100 ºF. In the past 24 hours, she has had nine loose stools admixed with blood and mucus. She hasn’t had any nausea or vomiting. She is eating and drinking properly. Social and family history is not available. Her stool culture was positive for Shigella sonnei, which was resistant to trimethoprim-sulfamethoxazole, ampicillin and ticarcillin. A five-day course of Cefixime was initiated. From 12/31/01 to 2/12/02, twenty cases of S. sonnei have been isolated from stool cultures in The Johns Hopkins Hospital. All cases were resistant to ampicillin, 17 cases were resistant to trimethoprim-sulfamethoxazole, and 19 cases were sensitive to tetracycline, nalidixic acid, and amoxicilline / calvulanic acid.
Shigella sonnei
Organism characteristics and identification:
Shigella spp. are non-lactose fermenters, glucose fermenters, indole positive, urea and oxidase negative, non-motile, facultatively anaerobic, Gram negative rods, which belong to the family Enterobacteriaceae. There are four species of Shigella: S. dysenteriae (serogroup A), S. flexneri (serogroup B), S. boydii (serogroup C), and S. sonnei (serogroup D). In addition to serogrouping, S. sonnei can be distinguished from other Shigella species by the expression of ornithine decarboxylase. Diagnosis is made from stool cultures. Colonies that appear suspicious on low selectivity media such as MacConkey or eosin methylene blue (EMB), are subcultured onto selective media such as Salmonella-Shigella (SS), xylose-lysine-deoxychoclate (XLD), or hekton enteric (HE). On triple sugar iron agar, colonies that are Shigella give an alkaline slant, acid at the bottom (due to glucose fermentation), without gas or hydrogen sulfide production.
Clinical presentation:
Shigellosis is a descending intestinal tract infection and typically
presents with high fever, abdominal cramps and watery and / or bloody,
mucoid diarrhea, without nausea or vomiting. The average incubation period
is 3 days (range of 1-7 days). Small intestinal involvement is associated
with voluminous watery stool whereas colonic involvement presents with
frequent small volume stool. In a healthy host, the infection is generally
self-limited, and without treatment, resolution of infection usually occurs
within 7 days. Complications may include seizures, leukemoid reaction,
dehydration, hyponatremia, intestinal perforation, obstruction and megacolon
(predominantly S. dysenteriae 1), hemolytic uremic syndrome (S.
dysenteriae 1), arthritis (S. flexneri) and rarely bacteremia.
Epidemiology:
Shigellosis has shown cyclic epidemic patterns of disease, each lasting 20-30 years. In the early years of 20th century, S. dysenteriae 1 was the common cause of shigellosis in Europe. Between 1926 and 1938, S. flexneri infection became more prevalent. Currently in Europe and the United States, S. sonnei is the most common cause of shigellosis. This cyclical pattern may reflect the development of population-based serotype specific immunity.
In the United States, between 1986 to 1996, the average incidence of shigellosis has been 10.8 cases per 100,000 population. In the United States the highest rate of shigellosis is seen in 1-4 year age group. Transmission of Shigella can occur via the fecal-oral route (person to person transmission), and contaminated food and water supply. In the United States most transmission occurs by the fecal-oral route, predominantly in day care centers and custodial institutions. Infected children from day care centers introduce the infection to their families, with the secondary attack rate of 20%. Outbreaks due to contaminated water or food have been reported. In January, 2000, at least 30 culture confirmed cases of S. sonnei infection associated with eating nationally distributed dip in California, Oregon, and Washington states was reported by CDC. A S. sonnei outbreak associated with contaminated drinking water occurred in Island Park, Idaho, in August 1995. In untreated cases, fecal excretion of the infecting strain generally lasts 1-4 weeks. Although uncommon, long term carriers of Shigella have been documented. The number of organisms shed by these individuals is less than what is seen in active cases.
Pathogenesis:
Due to its relative resistance to the stomach acid, as few as 10 to 100 organisms are sufficient to cause shigellosis. Shigella infection is generally limited to the intestinal mucosa. The organism can enter both enterocytes and M cells, which are specialized epithelial cells overlying mucosal lymphoid follicles. The infection process involves multiple steps including macropinocytosis, escape into the cytosol followed by multiplication, and passage to the adjacent cells. The Ipa proteins, which mediate macropinocytosis, are encoded on the "virulence plasmid". Shigella strains produce 3 distinct enterotoxins: the virulence plasmid encoded ShET2 by all four species, chromosomally encoded ShET1 by S. flexneri 2a strain, and phage-borne Shiga toxin by S. dysenteriae 1. The exact contribution of the enterotoxins in the disease process is not clear, since non-toxigenic strains of Shigella can cause significant disease. The acute inflammatory response by the host to Shigella infection, with the accompanying generation of cytokines, contributes to the disease process.
Treatment:
In the absence of susceptibility information, the treatment of choice for shigellosis is trimethoprim-sulfamethoxazole. In certain areas of the World, where trimethoprim resistance commonly occurs, ciprofloxacin, norfloxacin, nalidixic acid (children) or azithromycin may be used.
References:
Copyright © 2002 THE JOHNS HOPKINS UNIVERSITY