Bacillary Dysentery
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Bacillary Dysentery
1
DEFINITION •
Bacillary dysentery can be caused by many kinds of bacteria such as: • genus shigellae • enteroinvasive E.coli (EIEC) • campylobacter fetus subspecies jejuni: (helicobacter) etc.
2
Bacillary Dysentery •
Shigellosis is an acute bacterial infection caused by the genus shigellae, resulting in colitis, and affecting predominantly the rectosigmoid colon.
3
Bacillary Dysentery •
Shigellosis is characterized by fever, abdominal pain, diarrhea, tenesmus & dysentery. And in severe cases, infectious shock and /or toxic encephalopathy can be seen.
4
ETIOLOGY •
1.Shigellae are gram-negative bacilli belonging to the family Enterobacteriaceae. • 2. On the basis of antigenic & biochemical properties, shigellae are divided into four species: Group A S. dysenteriae Group B S. flexneri Group C S. boydii Group D S. sonnei 5
ETIOLOGY •
3. S.dysenteriae 1 causes epidemics with more severe clinical manifestations and higher mortality than other serotypes. • 4. Each type of shigella can release endotoxin which is responsible for the main toxic symptoms. S.dysenteriae can produce exotoxin (shiga toxin) that always exacerbate the clinical manifestations such as diarrhea. 6
EPIDEMIOLOGY •
1. Source of infection: patients & the carriers. • The atypical & chronic patients & the carriers are always out of attention because of their light symptoms, thereupon they are more important in epidemiology. 7
EPIDEMIOLOGY • •
2. Route of transmission: Shigellosis is transmitted by the fecal-oral route through contaminated hands, foods, water etc. • Transmission always occurs through close person-to-person contact. 8
EPIDEMIOLOGY • •
3. Susceptible group: All the people are susceptible to shigella but crowded living condition, poor water supply and other low standards of hygiene all contribute to an increased risk of infection. • Children have the greatest risk of developing shigellosis because of bad health habits. 9
EPIDEMIOLOGY • • •
4. Epidemic feature: Relapse & reinfection is common Summer & autumn
10
PATHOGENISIS & PATHOLOGY •
1.Since the microorganisms are relatively resistant to acid, shigllae pass the gastric barrier more readily than other enteric pathogens. About 200 bacilli can produce shgellosis, which is much fewer than typhoid & cholera. 11
PATHOGENISIS & PATHOLOGY •
2. During the incubation period(usually 12 to 72h), the organisms tranverse the small bowel, penetrate colonic epithelial cells, and multiply intracellularly & then lead to an acute inflammatory response. After the epithelial cells containing bacteria are lysed, there come the superficial ulcerations . 12
PATHOGENISIS & PATHOLOGY •
3.Inflammation is confined to the rectum and rectosigmoid colon & in severe cases, there may be pancolitis. • 4. Diarrhea results from:
13
PATHOGENISIS & PATHOLOGY •
5.Bacteremia is infrequency. One reason is the ulceration is superficial(virulence), another is that shigella is susceptible to serum complement-mediated bacteriolysis. • 6.Toxic shigellosis always occur in those whose immunity is strong enough to kill great deal of shigellae or those who get in much endotoxin directly. 14
CLINICAL MANIFESTATIONS
•
1. The severity of shigellosis is mainly related to the different strain of infecting organism , and so as mortality rate. (S.dysenteriae.1)
15
CLINICAL MANIFESTATIONS •
2. Most patients with shigellosis begin their illness with a nonspecific prodrome. Fever, crampy abdominal pain, watery diarrhea are the most common early symptoms & coincide with infection of the small intestine. 16
CLINICAL MANIFESTATIONS •
The height of fever: varies from 38 to 40 degrees celsius. • Abdominal tenderness: often marked in the left lower quadrant over the sigmoid colon but may also be generalized, always with the sensation of bowel movement & the feeling will not disappear after defacation. 17
CLINICAL MANIFESTATIONS •
Frequency and volume of diarrhea varies too, mainly basing on the destruction of local mucosa by shiga toxin. This phase of illness lasts for several days in most patients.
18
CLINICAL MANIFESTATIONS •
With the infection of colon, tenesmus, fecal urgency & the passage of bloody mucoid stools occur. • The amount of blood on the stools is usually small.
19
CLINICAL MANIFESTATIONS •
3. Patients with mild disease develop only prodrome or experience only watery diarrhea without dysentery. • 4. In severe cases, dehydration, electrolyte disturbance, acidosis, circulatory failure, unconsciousness etc. can be present, which are often the causes of death, especially in children. 20
CLINICAL MANIFESTATIONS
•
Shigellosis can be acute or chronic. • Shigellosis lasts more than 2 months is chronic and usually caused by group B. 21
LABORATORY TESTS •
Bloody and purulent are grossly apparent in severe bacillary dysentery. • Even in milder cases, microscopic examination of the stool often reveals numerous leukocytes and erythrocytes.
22
LABORATORY TESTS •
The presence of a bundant polymorphonuclear leukocytes helps in distinguishing shigellosis from diarrhea syndromes caused by viruses & enterotoxigenic bacteria. • The fecal leukocyte examination is not helpful in distinguishing shigellosis from diarrhea illness caused by other invasive enteric pathogens (such as salmonella, campylobacter & Yersinia etc.). 23
LABORATORY TESTS •
The peripheral white cell count is of little diagnostic value, since it may range from less than 3000 to more than 30,000. • Sigmoidoscopic examination reveals diffuse erythema, with a mucopurulent layer and mucosa with shallow ulcers 3 to 7 mm in diameter. 24
DIAGNOSIS • • • • •
Shigellosis should be considered in any patient with acute onset of fever and diarrhea: Epidemiology History Examination of the stool is essential Definitive diagnosis depends upon shigellae isolation. (usually for three successive days) 25
TREATMENT
•
The correction of fluid, electrolyte & acid-base disturbances are the mainstay of therapy & particularly important in elderly & very young patients. 26
TREATMENT •
Antibiotics: Fluoroquinolones such as norfloxacin & ciproxacin are the most effective drugs.(not approved for pediatric use because of the side-effect on epiphysis growth). • No quinolone resistance was encountered • Contraindications: children, pregnant women etc. 27
TREATMENT
•
Trimethoprim-sulfamethoxazole(80 mg & 400 mg respectively each tablet): • 5 days both for adults & children • 2 tablets bid p.o. for adults • 10 mg/kg/day & 50 mg/kg/day respectively for children 28
TREATMENT
• Amipicillin: • 0.5 q.i.d p.o. • For 5 days • Effective for sensitive organisms
29
TREATMENT
•
Antiperistaltic agents should be avoided.
30
PREVENTION •
The most important control measure is to institute proper sanitary & hygienic measures. • Hand washing is extremely important in decreasing direct transmission. • Asymptomatic and convalescent carriers should be excluded from food preparation and handling. • A live attenuated oral vaccine is under development. 31
32
1
DEFINITION •
Bacillary dysentery can be caused by many kinds of bacteria such as: • genus shigellae • enteroinvasive E.coli (EIEC) • campylobacter fetus subspecies jejuni: (helicobacter) etc.
2
Bacillary Dysentery •
Shigellosis is an acute bacterial infection caused by the genus shigellae, resulting in colitis, and affecting predominantly the rectosigmoid colon.
3
Bacillary Dysentery •
Shigellosis is characterized by fever, abdominal pain, diarrhea, tenesmus & dysentery. And in severe cases, infectious shock and /or toxic encephalopathy can be seen.
4
ETIOLOGY •
1.Shigellae are gram-negative bacilli belonging to the family Enterobacteriaceae. • 2. On the basis of antigenic & biochemical properties, shigellae are divided into four species: Group A S. dysenteriae Group B S. flexneri Group C S. boydii Group D S. sonnei 5
ETIOLOGY •
3. S.dysenteriae 1 causes epidemics with more severe clinical manifestations and higher mortality than other serotypes. • 4. Each type of shigella can release endotoxin which is responsible for the main toxic symptoms. S.dysenteriae can produce exotoxin (shiga toxin) that always exacerbate the clinical manifestations such as diarrhea. 6
EPIDEMIOLOGY •
1. Source of infection: patients & the carriers. • The atypical & chronic patients & the carriers are always out of attention because of their light symptoms, thereupon they are more important in epidemiology. 7
EPIDEMIOLOGY • •
2. Route of transmission: Shigellosis is transmitted by the fecal-oral route through contaminated hands, foods, water etc. • Transmission always occurs through close person-to-person contact. 8
EPIDEMIOLOGY • •
3. Susceptible group: All the people are susceptible to shigella but crowded living condition, poor water supply and other low standards of hygiene all contribute to an increased risk of infection. • Children have the greatest risk of developing shigellosis because of bad health habits. 9
EPIDEMIOLOGY • • •
4. Epidemic feature: Relapse & reinfection is common Summer & autumn
10
PATHOGENISIS & PATHOLOGY •
1.Since the microorganisms are relatively resistant to acid, shigllae pass the gastric barrier more readily than other enteric pathogens. About 200 bacilli can produce shgellosis, which is much fewer than typhoid & cholera. 11
PATHOGENISIS & PATHOLOGY •
2. During the incubation period(usually 12 to 72h), the organisms tranverse the small bowel, penetrate colonic epithelial cells, and multiply intracellularly & then lead to an acute inflammatory response. After the epithelial cells containing bacteria are lysed, there come the superficial ulcerations . 12
PATHOGENISIS & PATHOLOGY •
3.Inflammation is confined to the rectum and rectosigmoid colon & in severe cases, there may be pancolitis. • 4. Diarrhea results from:
13
PATHOGENISIS & PATHOLOGY •
5.Bacteremia is infrequency. One reason is the ulceration is superficial(virulence), another is that shigella is susceptible to serum complement-mediated bacteriolysis. • 6.Toxic shigellosis always occur in those whose immunity is strong enough to kill great deal of shigellae or those who get in much endotoxin directly. 14
CLINICAL MANIFESTATIONS
•
1. The severity of shigellosis is mainly related to the different strain of infecting organism , and so as mortality rate. (S.dysenteriae.1)
15
CLINICAL MANIFESTATIONS •
2. Most patients with shigellosis begin their illness with a nonspecific prodrome. Fever, crampy abdominal pain, watery diarrhea are the most common early symptoms & coincide with infection of the small intestine. 16
CLINICAL MANIFESTATIONS •
The height of fever: varies from 38 to 40 degrees celsius. • Abdominal tenderness: often marked in the left lower quadrant over the sigmoid colon but may also be generalized, always with the sensation of bowel movement & the feeling will not disappear after defacation. 17
CLINICAL MANIFESTATIONS •
Frequency and volume of diarrhea varies too, mainly basing on the destruction of local mucosa by shiga toxin. This phase of illness lasts for several days in most patients.
18
CLINICAL MANIFESTATIONS •
With the infection of colon, tenesmus, fecal urgency & the passage of bloody mucoid stools occur. • The amount of blood on the stools is usually small.
19
CLINICAL MANIFESTATIONS •
3. Patients with mild disease develop only prodrome or experience only watery diarrhea without dysentery. • 4. In severe cases, dehydration, electrolyte disturbance, acidosis, circulatory failure, unconsciousness etc. can be present, which are often the causes of death, especially in children. 20
CLINICAL MANIFESTATIONS
•
Shigellosis can be acute or chronic. • Shigellosis lasts more than 2 months is chronic and usually caused by group B. 21
LABORATORY TESTS •
Bloody and purulent are grossly apparent in severe bacillary dysentery. • Even in milder cases, microscopic examination of the stool often reveals numerous leukocytes and erythrocytes.
22
LABORATORY TESTS •
The presence of a bundant polymorphonuclear leukocytes helps in distinguishing shigellosis from diarrhea syndromes caused by viruses & enterotoxigenic bacteria. • The fecal leukocyte examination is not helpful in distinguishing shigellosis from diarrhea illness caused by other invasive enteric pathogens (such as salmonella, campylobacter & Yersinia etc.). 23
LABORATORY TESTS •
The peripheral white cell count is of little diagnostic value, since it may range from less than 3000 to more than 30,000. • Sigmoidoscopic examination reveals diffuse erythema, with a mucopurulent layer and mucosa with shallow ulcers 3 to 7 mm in diameter. 24
DIAGNOSIS • • • • •
Shigellosis should be considered in any patient with acute onset of fever and diarrhea: Epidemiology History Examination of the stool is essential Definitive diagnosis depends upon shigellae isolation. (usually for three successive days) 25
TREATMENT
•
The correction of fluid, electrolyte & acid-base disturbances are the mainstay of therapy & particularly important in elderly & very young patients. 26
TREATMENT •
Antibiotics: Fluoroquinolones such as norfloxacin & ciproxacin are the most effective drugs.(not approved for pediatric use because of the side-effect on epiphysis growth). • No quinolone resistance was encountered • Contraindications: children, pregnant women etc. 27
TREATMENT
•
Trimethoprim-sulfamethoxazole(80 mg & 400 mg respectively each tablet): • 5 days both for adults & children • 2 tablets bid p.o. for adults • 10 mg/kg/day & 50 mg/kg/day respectively for children 28
TREATMENT
• Amipicillin: • 0.5 q.i.d p.o. • For 5 days • Effective for sensitive organisms
29
TREATMENT
•
Antiperistaltic agents should be avoided.
30
PREVENTION •
The most important control measure is to institute proper sanitary & hygienic measures. • Hand washing is extremely important in decreasing direct transmission. • Asymptomatic and convalescent carriers should be excluded from food preparation and handling. • A live attenuated oral vaccine is under development. 31
32
