Theme Shigellae infections. Salmonellae infections. Escherichia infections. Yersiniosis. Rotaviral infection Theme Viral hepatitis A, B, С, d et al. Gastrointestinal infections: guidance, data and analysis
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Lesson 14 Theme 1. Shigellae infections. Salmonellae infections. Escherichia infections. Yersiniosis. Rotaviral infection Theme 2. Viral hepatitis A, B, С, D et al. Gastrointestinal infections: guidance, data and analysis
Yersiniosis - Protocol - Government of Manitoba Hepatitis A: guidance, data and analysis
SHIGELLA Shigella infections (dysenteries) are acute human Infectious Diseases with fecal- oral transmitting that are characterized by colitic syndrome and symptoms of general intoxication, quite often with development of primary neurotoxicosis.
pathogens. These organisms are members of the family Enterobacteriaceae and tribe Escherichieae; they are grouped into 4 species: Shigella dysenteriae, Shigella flexneri, Shigella boydii, and Shigella sonnei, also known as groups A, B, C, and D, respectively.
They are nonmotile, non – spore forming, rod shaped, and nonencapsulated, produce endotoxin, are resistant to the environment (in milk, water, food stays for several days, in soil - for several weeks), are stable to the freezing, but sensitive for boiling. Subgroups and serotypes are differentiated from each other by their biochemical characteristics (e.g., ability to ferment D-mannitol) and antigenic properties. Group A has 15 serotypes, group B has 8 serotypes, group C has 19 serotypes, and group D has 1 serotype. Geographic distribution and antimicrobial susceptibility varies with different species. S dysenteriae serotype 1 causes deadly epidemics, S boydii is restricted to the Indian subcontinent, and S flexneri and S sonnei are prevalent in developing and developed countries, respectively. S flexneri, enteroinvasive gram-negative bacteria, is responsible for the worldwide endemic form of bacillary dysentery.
• Contagious patient • Bacillus carrier The disease is communicable as long as an infected person excretes the organism in the stool, which can extend as long as 4 weeks from the onset of illness. Bacterial shedding usually ceases within 4 weeks of the onset of illness; rarely, it can persist for months. Appropriate antimicrobial treatment can reduce the duration of carriage to a few days. Shigella is spread through fecal-oral mechanism of transmitting. The way of transmitting • Contact • Alimentary • Watery
Vectors like the housefly can spread the disease by physically transporting infected feces.
Susceptibility: 60-70 % especially infants and preschoolers. The infectivity dose (ID) is extremely low. As few as 10 S dysenteriae bacilli can cause clinical disease, whereas 100-200 bacilli are needed for S sonneior S flexneri infection.
Pathogenesis: Shigella bacteria invade the intestinal epithelium through M cells and proceed to spread from cell to cell, causing death and sloughing of contiguously invaded epithelial cells and inducing a potent inflammatory response resulting in the characteristic dysentery syndrome. In addition to this series of pathogenic events, only S dysenteriae type 1 has the ability to elaborate the potent Shiga toxin that inhibits protein synthesis in eukaryotic cells and that may lead to extraintestinal complications, including hemolytic-uremic syndrome and death. Invasion of M cells, the specialized cells that cover the lymphoid follicles of the mucosa, overlying Peyer patches, may be the earliest event.
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Entering Shigella to gastrointestinal tract. 2.
Destruction of them under the influence of enzymes. 3.
Toxemia. 4.
Toxic changes in organs and systems (especially in CNS). 5.
Local inflammatory process (due to colonizing of distal part of the colon). 6.
Diarrhea.
Morphological changes in shigellosis Classification I. Clinical Form Typical • With dominance of toxicosis • With dominance of local inflammation • Mixed
Atypical • Effaced • Dyspeptic • Subclinical • Hypertoxic II. Severity (mild, moderate and severe) III. Course
• Acute (up to 1.5 mo) • Subacute (up to 3 mo) • Chronic (about 3 mo) - recurrent - constantly recurring IV. Presence of complications • uncomplicated • complicated V. Bacillus carrying Clinical criteria (typical form with dominance of toxicosis): • The incubation period varies from 12 hours to 7 days but is typically 2-4 days; the incubation period is inversely proportional to the load of ingested bacteria. • Toxic signs occur primarely (febrile temperature 39-40 °C, lose of appetite, vomiting, headache, fatigue) even may develope neurotoxicosis (hallucinations, unconsciousness, seizures). • Colitis is secondary (abdominal pain, tenesmus, false urge to defecate, sigmoid colon is tender, spastic, anus is open in severe cases. Feces in the form of a spit of mucus and blood (rectal spit), defecation are multiple). • Dehydration is not typical (except infants). Marble skin in toxicosis Clinical criteria (typical form with dominance of local inflammation) • Sudden onset from high-grade fever. • Abdominal cramping. • Sbdominal pain. • Tenesmus. • A large-volume, initially watery diarrhea with mucus, cylindrical epithelial cells • Later develops incontinence of feces, and mucoid diarrhea with frank blood as a rectal spit.
False urge to defecate Typical color of feces in shigellosis, rectal spit Sunken abdomen Rectal prolapse Peculiarities of Shigella infection in infants: • Acute beginning with slow development of signs and symptoms (for 3-5 days). • Distal colitis is less common. • Enterocolitis is more common, hemocolitis is rare. • Hepato- and splenomegaly. • Crying, anxiety, red face during defecation are equivalent to tenesmus. • Always gaping anus, sphincteritis occurs. • Dehydration is more common. • Course of the disease is prolongated.
Mild form • Subacute or acute onset of diarrhea • Stool 5-8 times daily with mucus and blood • Temporary pain in abdominal region • The temperature is normal or low febrile • Loss of appetite • Vomiting may occur Moderate form • Acute onset of diarrhea • Symptoms of toxicosis • The temperature is 38-39 °C • Anorexia • Crampy abdominal pain • Stool is 10-15 times daily • Pain during palpation in left inguinal region • Hepatomegaly Severe form • Multiple vomiting with bile, sometimes – as coffee lees, not only after meal, but also independently. • Defecation more than 15 times daily, sometimes – with each diaper, much mucus, blood, sometimes an intestinal bleeding developes. • General condition is severely worsened. • Quite often – sopor, loss of consciousness, seizures. • Changes in all organs and systems. • Severe toxicosis, dehydration (in infants). • Significant weight loss. Laboratory tests: o The white blood cell count: is often within reference range, with a high percentage of bands. Occasionally, leucopenia or leukemic reactions may be detected. o In HUS: anemia and thrombocytopenia occur. o Stool examination: fecal blood or leukocytes, mucus, cylindrical epithelial cells (confirming colitis) are detectable. o Stool culture: Specimens should be plated lightly onto Endo-Levin, Ploskirev, McConkey, xylose-lysine-deoxycholate, or eosin-methylene blue agars. o Blood culture: should be obtained in children who appear toxic, very young, severely ill, malnourished, or immunocompromised because of their increased risk of bacteremia. o Serological test: (AT, PHA in dynamics with 4-fold titer increasing in 10-14 days) in children elder than 1 year if fecal culture is negative. o Enzyme immunoassay: An enzyme immunoassay for Stx is used to detect S dysenteriae type 1 in the stool. o Rapid techniques: With rapid techniques, gene probes or polymerase chain reaction (PCR) primers are directed toward virulence genes (invasion plasmid locus).
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severe degree, acute course, uncomplicated. •
inflammation), moderate degree, constantly recurring course, complicated by the rectum prolapse. Differential diagnosis should be performed with: Salmonella infection, Escherichiosis, Acute appendicitis, Intestinal intussusception, Krohn’s disease, Nonspecific necrotizing colitis.
Criteria Functional Diarrhea Salmonella infection Shigella infection Epidemi o- logical anamne sis Sporadic diseases on the background of wrong feeding, care, etc. More often a group illness, connected with source of infection (products, contact with ill person or carrier of salmonellas) Both a sporadic, or a group illness, contact with ill person, connection with infected products Etiology Enzymopathy or motor function disability Salmonella Shigella Fever subfebrile (2-3 days), or normal 7 days and more 5-7 days and more
Not typical Moderate or severe, 5-7 days, prevails on diarrhea Mild to severe for 3-7 days, precedes intestinal manifestations
mild, or absent Moderate or severe, long- lasting Only in infants Course 2-3 days 7-30 days 7 and more days Feces Looks like chopped eggs, liquid
Dark-green with mucus (as mud), with blood Big amount of mucus, sometimes – blood and pus – rectal spit Vomiting Short (1-2 days), or absent Moderate and long-lasting (5-7 days)
Severe, but is not long
m (abdomin al distension) Mild, short (1-2 days) Always is present, long- lasting Abdomen is sunken Koprogram Typical for enzymopathy Mainly enzymopathy or Inflammatory changes Inflammatory changes Liver Is not enlarged Is enlarged Can be enlarged Spleen Is not enlarged Is enlarged Is not enlarged Criteria Escherichiosis Staphylococcal enterocolitis Viral diarrhea Epidemi o- logical anamne sis Sporadic diseases of infants, mainly hospital infeection, contact with ill person
Sporadic diseases of infants on a background of Staphylococcal infection of other organs, or Staphylococcal infection of the mother Group, or sporadic illness, with possble catarr of the upper respiratory tract
Etiology Pathogenic Escherichia Staphylococci Viruses (Rotavirus,etc.) Fever Is long-lasting (7-14 days), quite often – undulant Long-lasting subfebrile (for weeks, months) 3-5 days – high
Moderate, not less than 7 days, prevails over dyspeptic phenomena Mild, long-lasting (weeks, months) Moderate, 3-5 days
Often severe, long- lasting Absent, or mild Typical, severe
7-30 days Weeks, months 5-7 days Feces Not too frequent, colorless or brightly yellow, liquid, in a big amount Not too frequent, yellow, sometimes – with blood Watery (yellow, or rice- water), frequent
Moderate and long-lasting (5-7 days) Is absent Short (1-3 days), moderate Metheorism (abdominal distension) Severe, long-lasting Mild, but
long- lastin
g Moderate, short (1-2 days)
Enzymopathy or inflammatory changes Inflammatory changes Enzymopathy is possible Liver Is enlarged Is enlarged Is not enlarged Spleen Is not enlarged More often is enlarged Is not enlarged
• Water and food epidemiologic control. • Isolation and sanitation of ill person. • Convalescent may be discharged from the hospital after one negative feces culture (taken 2 days after the course of antibiotic therapy is finished). • Dispensary supervision of convalescents for 1-3 months. • Feces culture taken in contacted and carriers. • Supervision of contacted for 7 days, quarantine. • Disinfection of the focus of infection.
urge to defecate, gaping anus, spit of mucus and blood (rectal spit), sphincteritis.
SALMONELLA INFECTIONS Salmonella infection is an acute infectious disease of humans and animals that is caused by the numerous strains of Salmonella and more frequent courses as gastro-intestinal, rare – as typhoid and septic forms.
form capsules and spores. Their main antigents are O-, H-, and Vi-, by O-antigen they are devided on groups (A, B, C, D, E, F etc.). Most often Salmonella infection is caused by: • S. typhimurium • S. enteritidis • S. java • S. anatum and other Bacteria are stable in the environment (for months and years they live in food, water, soil), hot temperature kill them in 1 hour.
Epidemiology: •
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The transmitting of salmonellae to a susceptible host usually occurs via consumption of contaminated foods. The most common sources of salmonellae include beef, poultry, and eggs. Improperly prepared fruits, vegetables, dairy products, and shellfish have also been implicated as sources of Salmonella. In addition, human-to- human and animal-to-human transmittings can occur from amphibian and reptile chicks, ducklings, kittens, pet rodents, and hedgehogs.
The extension of the disease to various organs depends on the serotype, the size of the inoculum, and the status of the host. If large enough numbers of bacteria are ingested, they can survive in the normally lethal acidic pH of the stomach. Once ingested, Salmonella can gain access to the small intestine, producing diffuse mucosal inflammation, edema, and microabscesses. Generally, most nontyphoidal Salmonella (NTS) do not extend beyond the lamina propria and lymphatics of the gut. Exceptions include Salmonella choleraesuis and Salmonella dublin, which can cause bacteremia with little intestinal involvement.
In individuals with S. typhi, areas of intestinal necrosis can ulcerate and result in perforation. In addition, this mucosal penetration allows uptake into the draining lymph nodes, contributing to blood stream infections (BSI) and subsequent invasion of the liver, spleen, and bone marrow. This process explains the delayed onset of symptoms in S.typhi.
Schematically: 1. Massive entering of bacteria to the alimentary canal. 2. Destruction of salmonella in the upper parts of gastrointestinal tract. 3. Toxemia vomiting (as a protective factor). 4. Entering of other bacteria into small intestinum, colon, and colonization of epitheliocytes. 5. Local inflammatory process, dysperistalsis, development of indigestion and malabsorption, accumulation of biologically active substances, which impare absorption of water, electrolytes (diarrhea, dehydration). 6. Affection of the intestinal, lymphatic barriers (septic form of Salmonella infection). 7. Bacteriemia. 8. Forming of septic foci.
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Local form • Gastrointestinal form • Bacillus carrying 2. Generalized form • Typhoid fever-like form • Sepsis
3. Asymptomatic form II. Severity (mild, moderate and severe)
II. Course
• Acute (up to 1.5 mo) • Subacute (up to 3 mo) • Chronic (more than 3 mo) III. Presence of complications • uncomplicated • complicated IV. Bacillus carrying Clinical diagnostic criteria Of local gastro-intestinal forms: •
by direct contact); •
• intoxication (nausea, vomiting, high body temperature, headache); • abdominal pain; • diarrhea, usually appears secondary, stools are “muddy” (Pic. 201), may be with blood and mucus (Pic. 202), abdomen is tender; dehydration is moderate.
“Muddy” stools, hemocolitis
Typhoid form: • acute beginning from high temperature (39-40°C) lasting for 1-2 weeks; • vomiting, hallucinations; • “typhoid” tongue; • hepato-, splenomegaly from the 5-6 th day of the disease; • skin rashes (roseols) on the trunk on 8-10 th day;
• diarrhea; • tenderness in the right inguinal region of abdomen. Septic form: • Incubation period is long (5-10 days) • usually occurs in newborns, infants with predisposal factors (malnutrition, rickets etc.);
• is caused by antibiotic resistant, nosocomeal strains of Salmonella; • is transmitted by a direct contact with infected material; • acute beginning from fever that becomes hectic; • septic foci: meningitis, pneumonia, osteomyelitis, pyelonephritis, enterocolitis; • hepatosplenomegaly; • hemorrhagic syndrome; • development of toxic-dystrophic syndrome; • relapses; • prolonged course, bacillus carrying;
• high mortality. Salmonella infection in newborns • generalized form, high lethality are typical; • the mechanism of transmitting is contact (through nursery facilities); • the source of infection: infected mothers, personnel of the hospital; • agent: hospital strains of Salmonella; • high resistance to antibiotics; • latent period is prolonged (up to 5-10 days); • gradual beginning with growth of clinical symptoms; • severe and prolong intoxication;
• prolong course, formation of bacillus carrying, relapses of the disease; • development of a toxic-dystrophic syndrome. Laboratory tests • Complete blood count with differential: CBC count is often 10,000-15,000/μ L in simple gastroenteritis. Patients with typhoid form or sepsis commonly have anemia, thrombocytopenia, or neutropenia, although a shift to more immature forms can be seen on the differential count. • Cultures: Isolation of Salmonella from cultures of stool, blood, urine, or bone marrow is diagnostic. Specimens should be plated lightly onto Endo-Lewin, Ploskirev, McConkey, xylose-lysine-deoxycholate, or eosin-methylene blue agars. • Stool examination: Stool may be hemoccult positive and may be positive for fecal polymorphonuclear cells. • Chemistry: Electrolyte tests may reveal metabolic acidosis or other abnormalities consistent with dehydration. •
in children elder than 1 year if fecal culture is negative. Yüklə 3,37 Mb. Dostları ilə paylaş:
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