Home » Concept about enterotoxic and enteroinvasive diarrhea (salmonella, food poisoning caused by semi-pathogenic flora, esheryhiosis, cholera, yersiniosis, campylobacteriosis, shigellosis)

Concept about enterotoxic and enteroinvasive diarrhea (salmonella, food poisoning caused by semi-pathogenic flora, esheryhiosis, cholera, yersiniosis, campylobacteriosis, shigellosis)

June 6, 2024

Concept about enterotoxic and enteroinvasive diarrhea (salmonella, food poisoning caused by semi-pathogenic flora, esheryhiosis, cholera, yersiniosis, campylobacteriosis, shigellosis). Differential diagnosis of acute infectious and noninfectious diarrhea (mushroom poisoning, heavy metal salts, acute diseases of digestive system, gynecological and surgical diseases). Features of the differential diagnosis of botulism. Emergency states in acute diarrheal syndrome in the practice of infectious diseases, their treatment

Salmonellosis

http://www.webmd.com/food-recipes/food-poisoning/tc/salmonellosis-topic-overview

Salmonellae are widely dispersed in nature, being found in the in the gastrointestinal tracts of domesticated and wild mammals, reptiles, birds, and insects.

May present clinically as gastroenteritis, enteric fever, a bacteremic syndrome, or focal disease. An asymptomatic carrier state may also occur.

Pathogenesis

The development of disease after ingestion of Salmonella is influenced by the number and virulence of the organisms and by multiple host factors.

A large number of Salmonella must be swallowed in most instances to produce disease in healthy human being. However, in the event of infection with unusually virulent organisms or in patients with reduced resistance, symptomatic infection may result from extremely small inocula. Ingested organisms pass from the mouth to the stomach. In the stomach Salmonella are exposed to gastric acid and low PH, which reduce the number of viable organisms. Most Salmonella are perished rapidly at 2,0 PH, which is readily achieved in the normal stomach. Viable bacilli that survive then pass into the small intestine, where the organisms may be further reduced iumber or eliminated entirely. The antimicrobial activity observed in the small bowel is related at least in part to the normal microbial flora of the intestine, which elaborate short-chain fatty acids and perhaps other substances capable of killing or inhibiting growth of Salmonella. Studies in animals have shown that the increased susceptibility to Salmonella infection produced by administration of antibiotics rapidly reverts to normal with reestablishment of the normal intestinal flora.

Lactose-negative colonies of salmonella growing on MacConkey agar.

Salmonella that survive the antibacterial mechanisms in the stomach and upper small bowel may multiply in the small intestine. Multiplication of Salmonella in the intestinal tract may be asymptomatic, associated only with transient excretion of organism in stools, or symptomatic, associated with clinical manifestations of either enterocolitis (acute gastroenteritis) enteric fever or bacteremia.

Blood stream invasion, which occurs with variable frequency, may lead to localization of infection and suppuration at almost any site.

Local factors in the stomach and upper intestinal tract are important determinants of the disease. Factors that neutralize the low PH of the stomach or decrease the time the pathogen is exposed to stomach acid diminish local bactericidal action and increase the probability that an infections inoculums will reach the small intestine. The importance of gastric acidity as a defense mechanism is emphasized by the increased incidence of severe Salmonella enterocolitis in persons with achlorhydria, prior gastroectomy, gastroenterostomy, or vagotomy, conditions that reduce acidity or cause faster gastric emptying time.

The oral administration of buffering compounds also increases susceptibility to intestinal infection. It has been suggested that ingestion of organisms in food allows for longer exposure to gastric acid, thereby necessitating the presence of a relatively larger inoculums to produce disease, whereas water or other liquids, which have a fast gastric transit time, may be less heavily contaminated and still cause disease.

The small intestine provides other protective mechanisms through motility and normal flora. Alteration of the intestinal flora by antibiotics markedly reduces the size of the inoculums required to produce Salmonella infection in animals and humans and prolongs the convalescent carrier state. Prior antimicrobial therapy also enhances the possibility of infection with antibiotic – resistant Salmonella strains.

Age is an important determinant of disease produced by Salmonella. Salmonella enterocolitis occurs with highest incidence in children less than 5 years old; newborns and infants less one year of age are especially susceptible. The influence of age on incidence may reflect immaturity of humoral and cellular immune mechanisms, diminished antibacterial action of the normal intestinal flora, a high frequently of fecal-oral contamination, or other factors. In some instances, increasing resistance with age is related to immunity consequent to previous exposure to the organism, even though disease has not been produced.

Patient with impaired cellular and humoral immune mechanisms are at increased risk for development of Salmonellosis. Impairments of host defenses caused by malnutrition, malignancy, infection with human immunodeficiency virus or therapeutic measures such as corticosteroid or immunosuppressive therapy also predispose to infection and disease.

Salmonella causing enterocolitis are thought to produce diarrhea by a true infection with mucosal invasion and possibly by elaboration of an enterotoxin that acts on upper intestinal transport. Salmonella invasion of intestinal mucosa may lead to local production of inflammatory exudates of mediators that stimulate electrolyte secretion and smooth muscle contraction.

There are two types of toxins: exotoxins and endotoxins. Exotoxins are the toxic products of bacteria which are actively secreted into environment. Endotoxins are toxic substances which are liberated only during the lysis of microbial cells. The principal factor responsible for development of this disease is endotoxical complex of Salmonella, but we should remember that these bacteria produce even exotoxins. Exotoxins and endotoxins have toxical properties.

Stages of salmonellosis development:

1. 1. Colonization (setting) of pathogenic organism in the place of the inculcation.

2. 2. Invasion and reproduction.

3. 3. Death of the pathogenic bacteria and endotoxins liberation.

Infectious process may stop at the stage of colonization due to unknown reasons. Invasion may be limited by nearest tissues. In majority cases it leads to development of gastrointestinal forms of Salmonellosis. For development of the first stage of pathogenesis of Salmonellosis the factors violating structural and functional state of gastrointestinal tract play important role (dysbacteriosis, hypovitaminosis and other). These conditions may promote to development of the disease even due to small quantity of bacteria in food-stuffs.

In salmonellosis the principal pathologoanatomical changes develop in the place of inoculation of the agent in the small intestine. Data about changes of small intestine in gastrointestinal forms of Salmonellosis may be received only as a result of its biopsy. But biopsy is not used in practice. Investigation of material during biopsy testifies dystrophical changes of epithelium, infiltration of epithelium of mucous membrane by macrophages. Increased quantity of interepithelial leukocytes, polymorphonuclear leukocytes and macrophages is marked.

Principal changes develop in lamina propria of mucous membrane of small intestine in Salmonellosis. These changes are accompanied by hyperemia, hemorrhages, edema and intensification of cell infiltration. At the same time the changes of the different parts of gastrointestinal tract develop. There is an acute inflammatory process, dystrophic changes of epithelium, edema, hyperemia and cell infiltration in stomach. There are dystrophy, erosions, hyperemia, edema in mucous of large intestine. Changes in all parts of gastrointestinal tract are transient. They are exposed to reverse development in clinical recovery of the patients.

Salmonellosis. Flash-shaped undermining ulcer with necrosis of the epithelium and extrusion of necrotic tissue, fibrin and mucus.

In half of the patients with Salmonellosis nonsharp violations of liver are marked. These changes are considered as compensatory mechanism.

In connection with sufficient efficiency of modern methods of treatment the fatal outcomes are rare. Dystrophic changes of parenchymatous organs were revealed in autopsy of deceaseds from gastrointestinal forms of Salmonellosis. These changes were direct cause of death. Inrarely, edema of the lungs and brain, hyperplasia of spleen and mesenteric lymph nodes may develop.

Clinical manifestation

http://www.mayoclinic.com/health/salmonella/DS00926/DSECTION=symptoms

In connection with considerable variability of clinical duration of Salmonellosis there are multitude classifications of this disease. The next classification is more comfortable for practice use:

1) 1) Localized (gastrointestinal) forms of Salmonellosis:

a) a) Gastritic variant;

b) b) Gastroenteritic variant;

c) c) Gastroenterocolitic variant.

2) 2) Generalized forms:

a) a) Typhus-like form;

b) b) Septic form (septicopyemia).

3) 3) Carrier state:

a) a) Acute carriers;

b) b) Chronic carriers;

c) c) Transitory carriers.

Clinical symptoms of Salmonellosis are studied sufficiently completely. Gastrointestinal forms of Salmonellosis are observed in most of cases of the disease. According data of different authors they occur from 79 to 85 %.

Incubation period is from 4-6 hours up to some days. Onset of the disease is an acute. Prodromal period is not typical or very short. Weakness, malaise, and slight chill characterize it. Then temperature increases to subfebrile in moderate and severe forms accordingly.

After ingestion of contaminated food or water, illness begins in many patients with nausea and vomiting; these symptoms usually resolve within a few hours. Myalgia and headache are common. The cardinal manifestation is diarrhea, which may vary from a few loose stools to fulminate diarrhea. In most cases, stools are loose, of moderate volume, without blood, swamp-like and bed smell.

In exceptional cases, the stools may be watery and of great volume (“cholera-like”), or, in other instances, of small volume and associated with tenesmus and gross blood (“shigellosis-like”). Temperature elevations to 38-39 °C are common, as are chills; both appear in the majority of patients in whom definitive diagnosis is established. Abdominal cramps occur in about two-thirds of the patient and are often localized to the periumbilical region or lower abdominal quadrants. Bowel sounds are increased and abdominal tenderness is present. At microscopic examination, stool show a moderate number of polymorphonuclear leukocytes and, occasionally, red blood cells. Cross blood is unusual but may be seen in severe cases. Peripheral leukocyte count is usually normal, although neuthrophilia with a shift to younger forms may be present.

The duration of fever is less than 2 days in the majority of cases. Diarrhea usually persists less than 7 days, although, rarely, gastrointestinal symptoms may last for several weeks. Prolonged fever and diarrhea suggest a complication or a different diagnosis.

Localization of pain in the right lower quadrant of the abdomen in patients with enterocolitis may lead to a diagnosis of acute appendicitis. At surgery, such patients may have normal appendices or occasionally acute appendicitis rarely with perforation.

Clinic of Salmonellosis is characterized by symptoms of damage of cardiovascular system. The basis of these violations is water-electrolytes loss and change of reological properties of the blood.

Changes in organs of respiratory systems are not typical for uncomplicated cases of gastrointestinal forms. But sometimes breathlessness may be observed.

Toxicosis takes place when localized forms of Salmonellosis. It is manifested by headache, pain in the muscles, mild ataxia, asymetric reflexes. Development of toxic encephalitis is possible.

Electrolyte and water depletion may be severe during illness, leading to hypovolemic shock. The disease is more severe in children, in seniors, and in patient with achlorhydria, gastroectomy, gastroenterostomy, sickle cell anemia, or other conditions that impair resistance to infection. The frequency of transient bacteremia is less than 5 % in adults. It is increased in children and in persons with severe preceded diseases. Bacteremia has been shown to occur in 8-16 % of infants and children of 3 years age or younger who are hospitalized with Salmonella enterocolitis. Salmonella intestinal infections has tendency to be prolonged in children, who continue to excrete agent in stool for a longer time than adults after subsidence of clinical manifestation of infection.

Salmonella enterocolitis may develop in hospitalized patients. The illness may be a nosocomial infection or it may result of activation of pre-existing asymptomic intestinal infection by antimicrobial therapy, of surgical diseases of abdomen or from other causes.

In one-two third of children over 5 years and adults positive cultures are observed during second or third week from the onset of the disease. In this time majority of the patients have no symptoms of the disease.

Salmonella can produce an illness characterized by fever and sustained bacteremia without manifestations of enterocolitis. This syndrome may be caused by any Salmonella serotypes. The clinical syndrome of Salmonella bacteremia is characterized by a hectic febrile course lasting for days or weeks. The organism is isolated from blood, but stool cultures are ofteegative. More than 70 % of cases of generalized forms of Salmonellosis begin as gastrointestinal form with dyspeptic manifestations. Then, in typhus like variant after subsidence of dyspeptic manifestations the disease acquires signs of typhus infection. The second febrile wave-like or incorrect type continues in most cases during 10-14 days. The principal symptoms of the period of climax of the disease are weakness, adynamia, severe headache, sleeplessness, pains of muscles and joints.

Typical typhus state is not characteristic for this variant of Salmonellosis. In majority of the patients enlarged liver and spleen, distantion of abdomen are observed.

Approximately, in 25 % of the patients scanty rose sports are observed. Rash appears on 4-10 day, sometimes later. In peripheral blood leukocytosis is observed only in early period of the disease. Then leukopenia is marked, but with neutrophilosis. Sometimes typhus like variant may be without appearances of gastroenteritis. The principal symptoms of beginning period in that cases are fever, chill, headache, weakness. In the period of climax adynamia, pale skin, injections of scleras are observed.

There are single rose spots on the skin of abdomen and chest. In this variant of generalized form of Salmonellosis relapses may observed, and rarely, complications, which are typical for typhus fever. Typhus like variant may be with temperate manifestations of intoxication and dyspeptic appearances, with short duration fever. There is marked catarrh, hyperemia of pharynx, laryngotracheobronchitis in these patients rarely.

Septic variant (septicopyemia) is sepsis of Salmonella etiology. The development of sepsis is evoked by sharp decrease of the immuneprotective strengths of the organism of the patient. This variant of generalized of Salmonellosis is characterized by acyclic development of the disease, prolonged fever, chills, sweating, hepatosplenomegaly, sometimes development of jaundice, plural purulent metastases in different organs and tissues.

Usually, the disease begins from manifestations of gastroenteritis. Then typical septicopyemia develops with hectic fever. The signs of influence of intoxication on central nervous system are marked from the first days of the disease. They are manifested by irritation, violations of sleep, motive trouble, sometimes delirium. The skin is pale. Rash may appear on the skin (petechias or large hemorrhages).

Diagnosis

Diagnostics of salmonellosis is performed on the basis of epidemiological, clinical and laboratory data. Bacteriological and serological methods are used for confirmation of salmonellosis. The main materials for bacteriological investigation are vomiting masses, water after irrigation of stomach, stool, blood, urine.

Serological investigations are used. These are reaction of agglutination (RA) (7-8^th day of the disease) and indirect hemagglutination (RIHA). RIHA is more sensitive. It gives positive results on the 5^th day of the disease. Diagnostical titer is 1:200. Serological investigation should be done in dynamics of the disease.

Rentgenology investigation shows the increasing of thick intestin.

Differential diagnosis

Differential diagnosis of salmonellosis is perform with other intestinal diseases – shigellosis, toxic food-borne infections, esherichiasis, cholera; with surgical diseases – appendicitis, pancreatitis, cholecyctitis, thrombosis of mesenterial vessels; gynecological pathology and with therapeutic pathology (myocardial infarction, chronic gastritis aggravation, enterocolitis, ulcerous disease), with acute gastroenteritis of viral origin (enteroviral, rotaviral etiology), poisoning by organic and inorganic poisons, poisoning by mushrooms.

Generalized forms of salmonellosis is necessary to differentiate from sepsis of different etiology, pneumonia, malaria, acute pyelonephritis, tuberculosis.

Treatment

http://emedicine.medscape.com/article/228174-treatment

The volume of medical actions depends on the clinical form and a stage of gravity of disease. At gastrointestinal form immediately wash out stomach and intestine with boiled water (isotonic solution of Sodium chloridum is the best) then give sorbents per os and give a warm drink. For restoration of hydro-electrolityc balance and normalization of circulatory disorders there should be indicated per os Glucosole or Rehydroni. Infusion therapy is indicated at expressed dehydration – Trisol, Quartasol, Lactasol. At severe stage of dehydratation one of the specified solutions is infused in vein with rate 80-120 mL/min, 5-10 L of solution is necessary on course of treatment. If hypotension and toxicosis are marked Prednisolon and Hidrocortizon, Polyglucin, Reopoliglycin are infused in vein. Pathogenetically 5 % solution of glucose is indicated with desintoxication purpose and restoration of power balance, a solution of sodium hydrocarbonat for acidosis correction, Heparin for improvement of reologic properties of blood, preparations of antiallergic action – calcii chloridi, Dimedrol, Tavegil, Indomethacin are proved at severe diarrhea (for downstroke of Prostaglandines synthesis), calcium gluconate. Antibiotics at gastrointestinal form of salmonellosis are not used.

However at syndrome of hemocolitis and lingering diarrhea Furazolidon is indicated in combination with fermental preparations – Festal, Panzynorm, Pancreatin, Mezym forte, Pancitrat, Vobensim. The broths of herbs has anti-inflammatory, disinfectant and astringent properties, and also properties raising organism reactivity. They are vitamin preparations, Pentoxyl, Methyluracil, Thymalin, Enterol-250 also indicated. Bificol, Colibacterin, Bifidumbacterin, Linex is used at intestinal dysbacteriosis.

At generalized form simultaneously with pathogenetic therapy there are indicated antibiotics – Levomycetin, Ampicillin, Monomycin, Gentamycini sulfas, Cefazolin (Kefzol), Cefotaxim (Claforan). At the septic form of disease antibiotics are better to infuse parenteraly. For sanitation of chronic carriers of salmonelas the specified antibiotics use in average therapeutic doses in combination with preparations stimulating nonspecific and immunological reactivity (Pentoxyl, Methyluracil, Splenin, Thymalin, T- activin).

CHOLERA

Cholera is an acute anthroponosic infectious disease with fecal-oral mechanism of transmission. Cholera is characterized by dehydration due to loss of the fluid with watery diarrhoea and vomiting. Cholera is concerned to the group of the diseases, which are submitted to “international medical-sanitary roles”.

Vibrio cholera

Pathogenesis

Cholera is cyclic infection with essential fermental systems damage of the enterocytes. Vibrions cholera enter the organism through the mouth with water or food. Some part of vibrions perishes under influence of acid medium of the stomach. Another part of vibrions enters small intestine. Intestine reproduction and destruction of vibrions is accompanied with discharge of large amount of endo- and exotoxic substances. There is no inflammatory reactions.

Cholera is characterized by dehydration due to loss of fluid and salts with watery stool and vomiting. Hypersecretory processes play the leading role in the mechanism of the diarrhea origin. These processes are promoted by activation of ferment adenylcyclase in the epithelial cells of the intestine under action of exotoxin-cholerogen and accumulation of cyclic-3-5-adenosinemonophosphates, leading to increase of secretion of electrolytes and water.

In cholera the loss of fluid with stool and vomiting reaches such a great volume in a short period, practically not met during diarrhea of other etiology. The general volume may exceed in some cases up to 2 times the body’s mass of the patient. The loss of electrolytes plays essential role in pathophysiology of cholera. So, loss of potassium may reach one third its content in the organism. It is manifested by disorder of function of myocardium, damage of kidneys and also paresis of the intestine. In cholera dehydration is isotonic. Fluid contains 135 mmole/L Na, 18 mmole/L K, 48 mmole/L HCO₃ and 100 mmole/L Cl (or 5g NaCl, 4g NaHCO₃ and 1g KCl in 1 liter of defecation’s. An acute extracellular isotonic dehydration develops in the patients with cholera. It is accompanied with decreasing of the volume of circulated blood and hemoconcentration, leading to hemodynamic disorders and violation of tissue metabolism. Hypovolemia, metabolic acidosis, hypoxia, thrombo-hemorrhagic syndrome and acute renal failure develops.

In accordance with classification WHO the patients with cholera may be divided on three groups:

1. The first degree of dehydration. There are the patients which have loss of fluid volume equaled to 5 % of body weight.

2. The second degree of dehydration. There are the patients which have loss of fluid volume equal to 6-9 % of body weight.

3. The third degree of dehydration. The patients which have loss of fluid volume over 10 % of body weight. That dehydration is dangerous for life if the reanimation measures are not entertained.

According to classification of V. I. Pocrovsky patients can be divided in four groups:

1. 1. The first degree of dehydration with loss of fluid 1-3 % of body weight.

2. 2. The second degree of dehydration with loss of fluid 4-6 % of body weight.

3. 3. The third degree of dehydration with loss of fluid 7-9 % of body weight.

4. 4. The fourth degree of dehydration with loss of fluid more then 10 % of body weight.

It’s worth to underline that the clinical manifestation of the third degree of dehydration (by the WHO classification) or the fourth degree (by classification of V. I. Pocrovsky) is hypovolemic shock.

Clinical manifestations

Clinical manifestations of cholera, caused by classic vibrion and vibrion El-Tor are similar.

Incubation period is from some hours till 5 days (in average 48 hours). Cholera may be present in typical and untypical forms. In typical course the next forms of the disease are differented in accordance with the degree of dehydration: light, moderate and severe form. In untipical course obliterated, fulminant forms may be present.

The onset of the disease is an acute, as rule. In light course of cholera the gradual development occurs in the part of the patients. The prodromal period may be 1-1.5 days. The patients mark weariness, ailing, headache, sometimes subfebrile temperature, heartbeating, sweet.

A diarrhoea is the first clinical manifestation of cholera. It appears suddenly, without the pain, often at night or in the morning. Diarrhoea is accompanied by gurgation in the stomach. After 1-2 defecation stool has typical shape. It is cloudy, white, fluid, without smell and “rice-water”.

“Rice-water” character of stool in cholera

There are no changes of the pulse and arterial pressure. An insignificant painfulment occurs due to palpation of the stomach. The changes of the blood are not typical. There is no blood’s condensation, change it’s pH and electrolytes.

After corresponding therapy a vomiting, dizziness, weakness disappear at the first day. The stool become normal on the 2-3 day of the treatment.

In moderate course (dehydration of the second degree) the loss of fluid is 4-6 %. There is considerable weakness, dizziness, and thirst in patients. A quantity of the defecation is from 10 till 20 times in a day. The stool is liquid, plentiful. Dehydration appears already after 3-5 defecation at the half of the patients. A vomiting is annexed early, and it is rice-water-like. The skin is pale. The moderate cyanosis of lips and extremities may be in the part of the patients. There is harsh voice. Turgor of the skin decreases. The feature of this degree of dehydration is appearance of the cramps without tonic tension. The pulse is frequent up to 100 per minute. The arterial pressure is decreases till 100 mm. May be olyguria.

There are no changes of the red blood. Erythrocyte sedimentation rate (ESR) is lightly accelerated. Leukocytosis, neutrophylosis with the shift of the formula to the left, lymphopenia, monocytopenia and uneosinophilia occur in the part of the patients. Hematocrit is 51-54 %. The relative density of the plasma is 1026-1029. The change of electrolytes is insignificant. Hypokalemia and hypochlorinemia are more expressed. Hypotension disappears usually through 20-30 minutes from the onset of rehydration. Turgor is restored through 3-4 hours. The skin becomes pink. A vomiting continues till a day. Rarely a vomiting is observed on the second day. The stool becomes facesic through 1-3 days, and it becomes normal to 4-5 day. The general loss of the fluid is 5-7 liters in this patients.

Severe course (dehydration of the third degree) occurs more rarely, approximately in 10 % of the patients. The loss of fluid is 7-9 % of body weight. The detachment this degree of dehydration is connected with necessity of prevention of development extremly severe course. There are no secondary changes of the important system of the organism due to this degree of dehydration. Because, it may be possible rapid compensation of dehydration and restoration of electrolytes. The third degree is characterized by more intensive clinical manifestations of dehydration and unfirm compensation.

The disease develops impetuously. The stool is watery, abundant from the first hours of the disease. Sometimes the patient cannot count a quantity of defecations. In patients sharp weakness, adynamia, severe thirst, cramps of the muscles are observed. The state of the patients is serious and very serious.

A cyanosis of lips and extremities is observed. The skin is cold and shriveled. The turgor decreases. The face is pinched, eyes are deeply sunken in the orbits. In a third of the patients a symptom of “black eyeglasses” is observed. The mucous of the mouth cavity is dry. The lips are dry too. Tongue is dry and covered. A voice becomes hoarse. The cramps are often of long duration, with tonic character. Cramps are accompanied with pain. The cramps of the trunk muscles and diaphragm are not observed. The temperature is 35.7-35.5 ºC. The pulse is 120-130 in a minute, weak. The arterial pressure is low 80/50 mm. Sometimes the breathlessness occurs. Renal failure is manifested by olyguria, in 25 % – by anuria. There are erythrocytosis, leucocytosis, neutrophylosis with the shift of the formula to the left, lymphopenia, uneosinophilia. The concentration of hemoglobin increases. Protein and leukocytes are observed in urine. Hematocrit is 55-65 L/L in these patients. The relative density of plasma is 1030-1035. There is considerable change of electrolytes. Hypokalemia, hypochlorinemia are expressive.

Severe degree of dehydration.

Extremly severe course (dehydration of the forth degree) or decompensated dehydration. It occurs more rarely than the other clinical variants. The loss of fluid is 10 % of body weight and more.

In this case the organism cannot compensate the indigence of water-electrolytes balance and function of the significant organs. It leads to hypovolemic shock. The relapsing vomiting is observed. Decompensated dehydration may develop through 6-8 hours and even at the first 2-3 hours. The state of the patients is serious and very serious. In the last hours diarrhoea and vomiting may be absent. It is connected with paresis of the stomach and intestine muscles, with hypokalemia and metabolic acidosis. At the same time there are expressive symptoms of dehydration: cold clammy skin, intensive total cyanosis.

The color of the hand’s clusters, nouse, aural areas, lips and eyelids is violet or black. The face is pinched, eyes deeply sunken in orbits. There is impression of the suffering and entreaty about help on the face (facies cholerica).

The skin is shriveled. The turgor of the skin is decreased (“washwoman’s hands”). A voice becomes hoarse. The temperature is 34.5 ºC. The generalized tonic muscles cramp are observed, including muscles of the abdomen and back. The agonizing hiccup may be due to clonic spasm of diaphragm. There is no pulse. The arterial pressure is not determined. The breathing is frequent and superficial. There is anuria. The condensation of the blood is observed. In peripheral blood the concentration of hemoglobin increases. Expressive leucocytosis, neutrophylosis, lymphopenia, uneosinophilia occur. Hematocrit is higher than 66 %. The relative density of the plasma is 1036 and more. The alterations of electrolytes are very expressive: hypokalemia, hypochlorinemia. Hyponatremia is expressed in a smaller degree. Dehydration has isotonic character. The deficit bicarbonium (more than 10mmol/l) leads to decompensated metabolic acidosis and respiratory alkalosis.

Untreated patients die. The cause of the death is an acute heart’s failure (at the first three days of the disease) or renal failure (up to 14-16 day).

Diagnosis

The bacteriological research of material from sick man or corpse is the principal method of laboratory diagnostics. The purpose of bacteriological method is detachment of cholera’s agent and it’s identification.

Special bed for patients with cholera.

The correct taking of the material has a great meaning for bacteriological research as the delivery of material to the laboratory. A quantity of the material is 0.1-0.2 gm, because the enormous quantity of the agent is contained at stool. It is necessary to take a bigger quantity of the agent from the patient with light form or carriers. The sowing is done to the dense or liquid nutritive mediums near patient’s bed. If there is no possibility delivering of the material to the laboratory, quickly, it is necessary adding of conservant, because vibrio cholera begins to perish already at the first 1-2 hours in usual conditions. An alkaline peptonic water is used for the sowing. The material for the sowing is necessary to take till beginning of the treatment. The preliminary answer may be through 12 hours, the final – through 24 hours.

The serological methods may be also used for diagnostics of cholera. There are methods of discovering antibodies to vibrio cholera in blood, the methods of detaching antigens of vibrio cholera at stool and other materials. At the last years luminescent-serological method is used. The result may be received through 1.5-2 hours.

Treatment

Patients needs immediate hospitalization in choleric department. They require emergency treatment which should be started at the pre-admission stage. It’s necessary to put them on special bed and indicate pathogenetic preparations with the purpose of compensation of liquid and electrolytes loss, and corrections of metabolic changes. Isotonic polyionic solutions – Trisol, Acesolum, Lactasol, Quartasol, Hlosol are indicated. Quartasol is more effective.

Quantity of liquid, which should be infused for initial rehydratation (during 1-2 hours), should correspond to stage of the organism dehydratation. At III and IV stages of dehydratation it makes accordingly 7-9-10 % of body weight and more. Polyionic solutions infuse in vein initially-stream introduction, then volumetric rate 70-120 mL/minutes. To infuse liquid with such rate, it is necessary to use simultaneously two and more systems for transfusion. Stream introduction of liquid is replaced by dropwise infusion after normalization of pulse, restoration the arterial blood pressure and normalization of body temperature, hemoconcentration and acidosis.

The next infusions of polyionic solutions is determined by rate of proceeding loss of water and salts. The compensatory rehydratation is provided during several days in severe cases. For definition of its volume it is necessary every 2 hours to determine quantity of excrements and vomitive masses to investigate clinical (a pulse rate, the arterial pressure, body temperature) and every 4 – 6 hours laboratory (relative density of blood plasma, haematocrite number, concentration of electrolytes in blood plasma and erythrocytes, PH, concentration of standard Sodii hydrogenii) parameters.

For prevention of side reactions of polyionic solutions preliminary warm up to 38 – 40 °С, at the first hours of treatment infuse Prednisolon 0,5 gm/kg per day. At infusion there is plenty of solution Trisol the metabolic alkalosis and hyperkalemia can be developed. In these cases infusion therapy is continued with solution Disol.

It cases of not compensated hypokalemia it is necessary to infuse preparations of potassium in addition. At a pernicious vomiting, cramps, anaphylactoid reaction there should be used Dimedrol or Suprastin with Promedol. As at patients with severe current of cholera the clotting develops, Cordiamin, coffein or epinephrin of hydrochlorid is contrindicated.

In case of I-II stages dehydration (liquid loss up to 6 % of body weight) and more severe dehydration is managed by intravenous injection of saline solutions, at absence of vomiting recommend to apply peroral indication of Glucosani in tablets or Rehydroni in packages 18,9 gm the content of 1 package dissolve in 1 L of boiled water and drink small portions.

Water-salt therapy should be over after appearance of excrements of normal character and at prevalence of quantity of urine over quantity of excrements in the last 6-12 hours.

Panangin or Asparcam during 1 mounth are indicated during early reconvalescence.

Antibiotics are the additional remedies. They accelerate clinical convalescence and prevent the further allocation of choleric vibrions. A preparation of a choice is Ciprofloxacin: 0,25-0,5 gm 2 times per day, in serious cases enlarge up to 0,75-2 times per day during 5-7 days or Erythromicin, or Laevomycetin. Tetracyclin and Doxycyclin, are effective. However, for the last years the majority of vibrio, allocated on territory of Ukraine, not sensitive to this antibiotic. For sanitation of vibrio carriers use the same antibiotics during 3-5 days.

Complication of rehydration

It may be pyrogenic reaction to solutions, hypokalemia, hyperkalemia.

Hypokalemia is observed more than 25 % of the patients with III degree of dehydration. The clinical manifestations are: distention of the stomach, pain in the stomach (hypokalemitic ileus).

Hyperkalemia develops in 15 % of the patients. The clinical manifestations are: red face and upper part of the body, cardialgia, typical changes of ECG, bradycardia. In this case it is necessary to inject Phillips solution №2. Phillip’s solution № 1 is injected again after signs of hyperkalemia elimination.

Etiotropic therapy is performed with antibiotics. Antibiotics cause shortening of diarrhoea duration and give possibility to decrease a quantity of fluid for injection.

Doxicycline is prescribed in dose 0,1 mg through 12 hours at the first day, than 0,3-0,5 mg through 6 hours during 3 days. Tetracycline is used for treatment of the patients with cholera in dose 0,3-0,5 mg through 6 hours during 5 days. It is possible to use chloramphenicol in 0,5 mg dose through 6 hours during 5 days.

Prophylaxis

The measures of prophylaxis depend on epidemic situation in the country. The information of world health organisation about cases of cholera in different countries has an important meaning.

The incidence of disease can be diminished by sanitary-hygienic measures, sanitary disposal of human faeces, purification and protection of water supplies, pasteurization of milk and milk products, strict sanitary supervision of preparation and siring of flood exclusion of persons with diarrhea from handling food, organization of the work about diseases of gastrointestinal tract and their examination on cholera.

Specific prophylaxis of cholera is performed by corpuscular vaccine and cholerogen-anatoxin.

Parenterally inoculated killed complete cell vaccine has been available for years, this vaccine stimulates high titers of serum vibriocidal antibodies, but it does not induce antibodies to toxin. Protection by vaccine has been induced for approximately 1 year, with vaccine efficacy approximately 70 %. Local gastrointestinal tract immunity against the organism and against the toxin should provide a better, less reactogenic immunogen using recombinant DNA technology an “attenuated” V. cholerae organism that lacks the genes for production of the A and B subunits of toxin was created. A plasmid containing the subunit gene was then constructed and inserted. Thus a candidate live V. cholera vaccine containing all the cell-was antigens necessary for adherence and the capacity to produce only the subunit of toxin has been engineered.

Food poisoning

http://www.nlm.nih.gov/medlineplus/ency/article/001652.htm

Toxic food-borne infections is an acute transitory disease, caused by conditionally pathogenic bacteria. These bacteria are capable to produce exotoxin (in food-stuffs). The disease is accompanied with symptoms of the damage of the upper parts of the gastrointestinal tract (gastritis, gastroenteritis) and by violation of the water-electrolyte balance.

Pathogenesis

In toxic food infections exotoxin is contained in food, besides bacteria. Due to this the incubation period is very short. Time of the of clinical manifestations development after influence of toxins to the mucous membrane is from 30 minutes till 2-6 hours.

Pathogenesis and clinical manifestations of the disease depend of the type and dose exotoxin, and also from other toxical substances microbial origin, containing in the food-stuff. Enterotoxins (thermoliable and thermostable) are connected with the epithelial cells of stomach and intestine and act to the fermental system of the epitheliocytes, but no cause morphological changes in these organs. Enterotoxin activates ferments adenylcyclase and guanylcyclase increasing formation of the biological active substance (cyclic adenosinemonophosphates and cyclic guanidinmonophosphates) in the cells of the mucous membranes. All these changes lead to the increase rate of secretion of water and salts into the stomach and intestine and to the development of diarrhea and vomiting.

Pathological anatomy

Cytotoxins damage the membranes of the epithelial cells and violates synthetic processes. It may increase the permeability of the intestinal wall for different types of the toxical substances, and for oneself microorganisms, development of intoxication and violation of microcirculation and localized inflammatory alterations of the intestinal mucous membrane.

Clinical manifestations

The clinical manifestations of the toxic food-borne infections caused by only enterotoxins are less severe. In the majority of the cases of the disease there is no fever and just considerable inflammatory changes of the mucous membrane of the stomach and intestine.

The course of the disease become more severe due to accumulation of enterotoxin and cytotoxin in the food-stuffs. The high fever and considerable change of the mucous membrane of the gastrointestinal tract are observed.

In toxic food-borne infections there is combination of the signs of the damage of the gastrointestinal tract (gastritis, gastroenteritis or gastroenterocolitis) and signs of the general intoxication and dehydration. The incubation period is from 30 minutes to 24 hours (generally 2-6 hours). The beginning of the disease is an acute. At first the nausea occurs. Frequently the replated, agonizing and unrestrained vomiting occurs. Almost at the same time with vomiting the diarrhea starts. Stool is watery from 1 to 10-15 times a day. In considerable part of patients the disease is not accompanied by severe pain in the stomach and increase of the body temperature of the body. However the disease may be with spasmatic pains in the stomach, with the raise of the body temperature upto 38-39 °C. The raise of the body temperature takes place at the early hours of the disease and through 12-24 hours the temperature is reduced to normal.

During objective examination of the patients the pale skin, sometimes cyanosis, cold extremities are observed. The tongue is coated. Stomach is soft and painful in the epigastrium during palpation. The cardiovascular system also suffers. There is bradycardia (during hyperthermia – tachycardia). The arterial pressure decrease. In some cases collapse of short duration develops. Due to repeated vomiting and plenty diarrhea the signs of dehydration develop. It may be possible of the appearance of the muscle’s cramps of extremities, decrease of the diuresis and reduced turgor of the skin. The liver and pancreas are not expanded. In hemogram leukocytosis, neutrophylosis and temperate accelerate ESR are noted.

The duration of the disease in majority of the cases is 1-3 days. The toxical food infection may be accompanied by severe complications. Hypovolemic shock and an acute heart insufficiency, connecting with violations of electrolytic balance (hypokalemia) are observed.

Diagnosis

The diagnosis of the toxic food-borne infections is made according the results of the clinical symptoms estimation, epidemiological and laboratory data. The typical signs are the impetuous development of the disease after short incubation period, presence of symptoms of gastritis, gastroenteritis or gastroenterocolitis in combination with intoxication, dehydration, disposition to the vascular dystonia.

It is necessary to consider the simultaneous disease of the group of the persons, use one itself food-stuff, the features of this product, sanitary-hygienic state of commercive institutions, public nutrition when taking epidemiologic data. It is necessary to reveal the sick men or bacteriocarries among personnel of these institutions, because they may be a source of infection of the food.

Materials for bacterial examination are suspicious food products, vomitory masses, water after irrigation of the stomach, stool of the patient. Serological methods does not have independent meaning in the diagnostics.

Differential diagnosis

Differential diagnosis of toxical food infection is performed with acute intestinal infections (cholera; acute shigellosis; gastrointestinal form of yersiniosis; rotoviral gastroenteritis; campylobacteriosis; dyspeptic variants of preicteric period of viral hepatitis and others), with surgical diseases (acute appendicitis; cholecystopancreatitis; thrombosis of mysentrical vessels; perforation of ulcers in the stomach and duodenum), with gynecological diseases (ectopic pregnancy; toxicosis of the pregnancy), with therapeutic diseases (myocardial infarction; hypertension crisis), with neurological diseases (acute damages of cranial blood circulation, subarachnoidal hemorrhage), with urological diseases (pyelonephritis; acute renal insufficiency). During the diagnostics it is necessary to consider the food poisoning; poisoning by mushrooms; salts of hard metals.

Treatment

http://www.nhs.uk/Conditions/Food-poisoning/Pages/Treatment.aspx

It is necessary to wash out a stomach and intestine to release them from microbes and toxins as soon as possible. For a lavage it is better to use isotonic solution of Sodium chloridum, boiled water or 1-2 % solution of sodium hydrocarbonate. Then give inside the activated microspherical coal (SKN brand). Alternative preparations are Sillard P, Smecta, Enterodes and other enterosorbents. Their early indication promotes the fastest improvement of health state, preserves intoxication, development of the serious form of bacterial endotoxicosis. In case of development of infection-toxic shock we should immediately infuse in blood colloid and cristaloid solutions: Polyglucin, Reopoliglycin, donor Albumin, Trisol, Acesol, Quartasol, and also glucocorticoides.

Etiotropic treatment is indicated only at serious forms with development of colitic syndrome: Furazolidon or Enteroseptol. Antibiotics are indicated in case of development of sepsis – Levomycetin, Gentamicin, Ampicillin, Ofloxacin (Tarivid).

Prophylaxis

Prophylaxis of the toxical food infection is concluded in prevention of infection of the food-stuff, of the reproduction of the microorganisms in the food. It is necessary to keep the food-stuffs and prepared food at the temperature from 2 till 4 ºC.

The mechanization and automatization of the food objects, the elaboration of the new methods of the preserving and storage of the food-stuff, the freezing at low temperature are conductive to the successful prophylaxis of the toxical food infection.

Shigellosis (dysentery)

http://science.jrank.org/pages/2193/Dysentery-Shigellosis.html

Shigellosis is general infectious disease of human, caused by bacterium of genus Shigella.

Shigellosis is characterized by principal damage of mucous membrane of distal section of the large intestine. The disease is accompanied by symptoms of general intoxication, abdominal spastic pain, frequent watery stool with admixture of mucus and blood, and tenesmus.

Pathogenesis

Pathogenesis of shigellosis is complicated. It is studied insufficiently. In some cases the agents perish in the upper section of the gastrointestinal tract under the influence of acidic conditions. In other cases Shigella may pass through intestine, and it is excreted into environment without reply of the macroorganism.

Diverse theories of pathogenesis of shigellosis were pulled out in different years. The next theories are known:

1. 1. Bacteriemic theory. Reproduction of the agent in the blood is the basis of pathogenesis of shigellosis according to this theory.

2. 2. Toxico-infections Shiga’s-Brauer’s theory. Many positions of this theory don’t lose one’s own meaning in modern ideas about pathogenesis of shigellosis.

3. 3. Allergic theory. According to this theory, shigellosis is general allergic infection disease.

4. 4. Nervous-reflexious theory. According to this theory the damage of nervous system has leading meaning in pathogenesis of shigellosis.

5. 5. Theory of intracellular parasitism. According this theory, all features of the shigellosis course are connected with parasitism of Shigella in the epithelium of mucous membrane of distal section of the large intestine.

In was established by investigations of the last years that secondary immune insufficiency plays considerable role in pathogenesis of shigellosis. At present time it is known that development and course of the different forms of shigellosis is connected with some factors. There are functional state of the organism; interaction of the human’s organism, agent and environment; biological properties of the agent (toxigenecity, invasiveness, fermentic activity and other).

Bacteremia of short duration may be observed in decreased resistance, in entering of the large doses of the agent. However, bacteremia hasn’t essential meaning in pathogenesis of shigellosis. Bacteremia is marked only in one third of the patients with Grigoriev’s-Shiga’s shigellosis.

Toxins, which are absorbed from the intestine, play an important role in pathogenesis of shigellosis. At first, toxins influence directly on the mucous membrane of the intestine and substances, disposing under mucous membrane (nervous endings, vessels, receptors). Second, toxins are absorbed and influence to different sections of central nervous system. Involvement of small intestine in pathological process from the first days of the disease is explained by toxinemia (violation of its motile, absorbing and digestive functions). The evidence of toxinemia is delivery of endotoxin into patient’s blood serum from the first days of the disease and its delivery into urine.

Exotoxin of Shigella Grigoriev’s-Shiga’s and protein part of endotoxin possesses significant neurotoxic action. Neurotoxins influence on the central nervous system and peripheral gangiums of vegetative nervous system. It is manifested by severe intoxicative syndrome and violation of all types of the balance of substances.

Lipopolysaccharide part of endotoxin damages principally mucous membrane of distal section of large intestine, and in a less degree, other sections of gastrointestinal tract. It possesses cytotoxic action and causes activation of adenylcyclase.

Activation of adenylatecyclase leads to accumulation of cyclic 3-5 adenosine-monophosphates, increased secretion of electrolytes and water. The violation of water – electrolytes balance is observed in gastrointeritic variants of acute shigellosis course. It is necessary to allow for degree of dehydration of the organism. Dehydration of II-III degree develops in severe course of gastroenterocolitic and gastroenteritic variant of acute shigellosis. In severe (hypertoxic) form it may be development of hypovolemic shock and acute renal insufficiency.

Shigella toxins cause sensibilization of the mucous membrane of the intestine, render damaging action on it with development of inflammatory changes and erosions formation and ulcers in severe course of the disease.

Toxin stimulates discharge of biological active substances (histamine, serotonine, kinines, prostaglandines) into blood, causes violation of microcirculation of the blood in the intestine’s wall, increases intensity of inflammatory process and disorders of functions of the intestine (motorics, absorbtion, secretion).

The violation of innervation of the intestine, microcirculation, electrolytic balance and inflammatory changes of mucous membrane are manifested clinically by sharp spastic pains in the stomach. Spasms of separate sections of the intestine lead to excretion of scanty stool (“fractional stool”). Spastic shortening of the muscles of sigmoid and rectum cause fecal urgency and tenesmus.

Allergic factor plays definite role in pathogenesis of shigellosis. Pathological process develops in large intestine after preliminary sensibility. However, it was shown experimentally, that shigellosis is not typical allergic disease.

However, intracellular parasitism was not confirmed due to biopsy of mucous membrane of the intestine in the patients with shigellosis. It is not expected, that phenomenon of intracellular parasitism plays certain role in shigellosis too.

In shigellosis, the invasion of Shigellas into epithelial cells is observed in large intestine, principally in rectum. It is caused by comparatively prolonged accumulation of intestinal content, toxins and bacteriums in the large intestine. They create favorable conditions for invasion of the agent into epitheliocytes. It is promoted by intestinal dysbacteriosis too. Intestinal dysbacteriosis develops inrarely under influence of antibioticotherapy. This therapy causes destruction of considerable part of symbiotic flora.

The disease may have prolonged or chronic course due to addition of supplementary factors of chronic process. The cases of formation of chronic shigellosis develops due to unfavorable premorbid state, delay of macroorganism functions replacement, decreased activity of immune system.

The recovery of the patients is prolonged in presence of damages at any portions of gastrointestinal tract (defects of masticatory apparatus, anomalies of intestinal tube, gastritis, ulcerous disease, appendicitis, pancreatitis, hepatitis, cholecystitis); presence of supplementary diseases (tuberculosis, brucellosis, malaria, helminthiases); state of endocrine system, dysbalance of vitamins. The factors, promoting to prolonged and chronic course of the disease, are late hospitalization of the patients, incorrect treatment, violation of alimentary regime after discharge of the patients from the hospital.

Complication of shigellosis (fall out of rectum)

There are the next clinical variants of acute shigellosis:

1. 1. colitic variant;

2. 2. gastroenterocolitic variant;

3. 3. gastroenteric variant.

Depending on gravity of the course of the disease there are mild, moderate and severe course of shigellosis, and also carriers.

Clinical manifestations

Colitic symptomocomplex is typical for shigellosis. Incubation period lasts from 2 till 5 days, rarely – 7 days.

Mild course. Onset of the disease is acute. The temperate pains appears in the lower part of the stomach, principally, in the left iliac area. These pains precede act of the defecation. Tenesmus are observed in some patients. Stool is from 3-5 till 10 times a day. It contains mucus, sometimes – blood. Temperature is normal or subfebrile. Catarrhic inflammation of mucous membrane is observed at rectorhomanoscopy, sometimes erosions and hemorrhages.

Moderate course. Onset of the disease is acute or with short prodromal period. It is characterized by weakness, malaise, discomfort in the stomach. Then, spasmatic pain appears in the lower part of the stomach, tenesmus. At first, stool has fecal character. Then, mucus and blood appear in stool. Stool loses fecal character and has appearance of “rectal spit” (excretion of scanty stool – “fractional stool”), with mucus and blood. Stool is accompanied by fecal urgency and tenesmus. Stool is from 10-15 times a day.

In patients with medium serious course of acute shigellosis temperature increases up to 38-39 °C for 2-3 days. Subfebrile temperature is possible. The patients complain of weakness, headache. It may be collapse, dizziness. The skin is pale. Hypotonia, relative tachycardia are observed. Tenderness and condensation of sigmoid are revealed. In the peripheral blood leukocytosis and temperate neutrophylosis are observed. In coprocystoscopy erythrocytes (more then 30-40 in the field of vision) are revealed. In rectorhomanoscopy diffusive catarrhic inflammation, local changes (hemorrhages, erosions ulcers) are revealed. In patients with moderate course of acute shigellosis functional and morphological restoration may be prolonged – till 2-3 months.

Severe course. Onset of the disease is acute. Temperature is increased up to 39 ˚C and higher. The patients complain of headache, harsh weakness, nausea, something vomiting. Strong abdominal spasmodic pains, frequent stool with smaller volume “without account”, with mucus and blood are marked.

There are hypotonia, harsh tachycardia, breathlessness, skin cyanosis. Harsh tenderness at the left iliac area, especially in the area of sigmoid are marked during palpation of the stomach. It is possible pasesis of intestine. There are expressive leukocytosis neutrophylosis with shift to the left. ESR is accelerated.

During microscopical examination of stool erythrocytes are marked through the field of the vision. In rectorhomanoscopy infusive catarrhic or fibrinous inflammation, presence of the local changes (erosions, ulcers) are marked. The functional and morphological restoration of intestine is longer than 3-4 months in patients after colitic variant of acute shigellosis.

Gastroenterocolitic variant of shigellosis. The principal feature of this variant of the acute shigellosis course is acute impetuous onset of the disease after short incubation period (6-8 hours). More frequent way of the transmission of the infection is alimentary. The factors of transmission are milk, milk products and other.

Intoxicative syndrome and symptoms of gastroenteritis are observed in the initial period. The manifestations of enterocolitis predominate in the period of climax.

There are mild, moderate and severe course of gastroenterocolitic variant of acute shigellosis. During estimate of the disease course gravity it is necessary to allow for not only degree of intoxication and damage of gastrointestinal tract, but also degree of dehydration, because repeated vomiting and plentiful diarrhea are observed. It may lead to dehydration of I-II-III degree.

Gastroenteritic variant of shigellosis. The principal feature of this variant of the acute shigellosis course is predominance of clinical symptoms of gastroenteritis and presence of certain degree dehydration symptoms. Nowedays, besides clinically distinct sings of the disease, lingering and obliterated course of shigellosis is observed. Obliterated course is characterized by insignificant clinical manifestations. The great ratio of the patients do not apply to physician. Careful bacteriological examination of the patient with different gastrointestinal disorders of unknown etiology has large meaning for correct diagnostics. In these patients catarrhic inflammatory changes of mucous membrane of distal portion of rectum is revealed in the majority of cases during rectorhomanoscopy.

Clinical recovery comes through 2-3 weeks in the majority of the patients with uncomplicated course of all variants of acute shigellosis. Complete functional and morphological restoration of gastrointestinal tract happens in 1-2 months and later. Relapses may arise in some part of the patients. The factors, promoting to relapses of the disease are the violation of diet, alcohol use, incorrect therapeutic tactics. The disease may have lingering course. Insufficient reactivity of the organism, sharp decrease of cell immunity in acute period of the disease promote to lingering course of shigellosis.

Lingering course of shigellosis. Shigellosis is estimated as lingering, if clinical manifestations of the disease are observed over 3-4 weeks. Declination to lingering course of the disease depends on gravity of the course of shigellosis in acute period. Colitic variant of severe course of acute shigellosis has prolonged course more frequently than moderate variant. The period of functional and morphological restoration of the intestine is over 3 months. In some patients lingering course is manifested only by persistent bacterioexcretion. Bacterioexcretion is combined with prolonged inflammatory process in rectum.

Bacterioexcretion. dysfunction of intestine is absent at the period of examination and preceded 3 months in presence of bacterioexcretion (subclinical bacterioexcretion) or excretion of Shigella after clinical recovery (reconvalescent excretion) in this form of infectious process.

a b c

Rectoromanoscopy in case of shigellosis and amebiasis:

a – catarrhal proctosigmoiditis

b – fibrinous-necrotic proctosigmoiditis

c, d – ulcer colitis (amebiasis)

Diagnosis

The principal methods of diagnostics of shigellosis are bacteriological and serological methods of investigation.

Excretion of coproculture of Shigella is more reliable method of confirmation of diagnosis of shigellosis. It is necessary to take the material for bacteriological investigation before beginning of the treatment.

Diagnosis may be confirmed by serological methods. Reaction of indirect agglutination with standard erythrocytic diagnosticum is used more widely. Diagnostic titer is 1:200 with increase of titer in 7-10 days.

Coprogramm (a lot of neutrophyles, erythrocytes in stool).

Treatment

http://www.azsymptoms.com/dysentery-symptoms.html#

The Complex of treatment is indicated, which depends on features of disease. In the first days the diet №4, and diet №2 (till clinical convalescence) are indicated.

At mild current of shigellosis etiotropic agents are not applied, at disease of average degree of gravity use basically preparations of Nitrofuranes: Furazolidon, Nifuroxasid 0.1 gr. 4 times per day. Use derivatives of 8-oxyquinoline – Enteroseptol, Intestopan, among other groups of preparations – Intetrix, Nalidix acid, Ftalazol. At ambulatory treatment of shigellosis with moderate stage of gravity Sulfanilamid preparations of prolonged action are indicated – Phthazin, Sulfadimethoxin.

In case of severe shigellosis current use antibiotics – Ampicillin or a Polymyxin; when there is no effect – Ciprofloxacin or Ofloxacin in combination with Gentamicin or Cefazolin are prescribed. Duration of course of etiotropic treatment at moderate current of shigellosis is 2 – 3 days, at severe case it lasts not longer than 4 – 5 days.

Solution of Regidron, in severe cases Quartasol, Lactosol are applying per os with the purpose of desintoxication and rehydratation. For the adsorption of bacterial toxins and metabolites from the intestine lumen and for their subsequent removing from the organism Enterodes, coal microspherical sorbents, Sillard P, Smecta are used. Rectal pollination with Sillard P in a dose 6 gm (1 – 3 procedures) is effective. There are proved Methyluracil, Pentoxyl, Thymalin as natural factors of nonspecific protection of the organism lysozyme and stimulators of regeneration. Calcy gluconate, Dimedrol, Suprastin, Tavegil is indicated as pathogenetic treatment.

According to parameters of coprocytogram use mono or polycomponental fermental preparations. At presence of plenty of fat drops in feces Pancreatin, Pancitrat, Pancurmen, and at detection of cellulose, Amyl, muscular fibers – Pansinorm, Festal, Mezym-forte, Abomin, Vobensim are applied.

There are indicated widely vitamins preparations, these are ascorbic acid, nicotinic acid, Thiamin chlorid, Riboflavin, Pyridoxine hydrochloride, Calcy Pangamat, folic acid, Rutin. It is better to use per os the balanced vitamin complexes – Dekamevit, Glutamevit.

Collibacterin, Bifidumbacterin, Bificol, Lactobacterin, Bactisubtil, Linex, Hilac forte, α – bacterin, Enterole-250 are indicated for elimination of intestinal dysbacteriosis and restoration of the normal biocenosis. Course of treatment is 2 weeks and longer.

Collectings of herbs and fruits of a bilberry, mint peppery, knot-herb ordinary, camomiles medicinal, herbs of a yarrow, centaury are helpful ordinary. Collecting with the shepherd’s bag ordinary, grasses of St.-Johns wort are effective at hemocolitis. Fermentative and putrefactive processes reduces at lingering colitis, that is why collecting of grass of a sage-brush, a horsetail field, grasses of a yarrow ordinary, roots of snakeweed are applied.

Broths and juices of herbs, oil of dog rose for microclysters after a cleansing enema, 0,5 % solution of a colloid silver as medical clysters, insufflations of Oxygen are used locally for stimulation of reparative processes in the mucosa of colon.

Cholera

http://www.nlm.nih.gov/medlineplus/ency/article/000303.htm

Pathogenesis

In cholera the loss of fluid with stool and vomiting reaches such a great volume in a short period, practically not met during diarrhea of other etiology. The general volume may exceed in some cases up to 2 times the body’s mass of the patient. The loss of electrolytes plays essential role in pathophysiology of cholera. So, loss of potassium may reach one third its content in the organism. It is manifested by disorder of function of myocardium, damage of kidneys and also paresis of the intestine. In cholera dehydration is isotonic. Fluid contains 135 mmole/L Na, 18 mmole/L K, 48 mmole/L HCO₃ and 100 mmole/L Cl (or 5g NaCl, 4gm NaHCO₃ and 1g KCl in 1 liter of defecation’s. An acute extracellular isotonic dehydration develops in the patients with cholera. It is accompanied with decreasing of the volume of circulated blood and hemoconcentration, leading to hemodynamic disorders and violation of tissue metabolism. Hypovolemia, metabolic acidosis, hypoxia, thrombo-hemorrhagic syndrome and acute renal failure develops.

In accordance with classification WHO the patients with cholera may be divided on three groups:

1. The first degree of dehydration. There are the patients which have loss of fluid volume equaled to 5 % of body weight.

2. The second degree of dehydration. There are the patients which have loss of fluid volume equal to 6-9 % of body weight.

3. The third degree of dehydration. The patients which have loss of fluid volume over 10 % of body weight. That dehydration is dangerous for life if the reanimation measures are not entertained.

According to classification of V. I. Pocrovsky patients can be divided in four groups:

5. 1. The first degree of dehydration with loss of fluid 1-3 % of body weight.

6. 2. The second degree of dehydration with loss of fluid 4-6 % of body weight.

7. 3. The third degree of dehydration with loss of fluid 7-9 % of body weight.

8. 4. The fourth degree of dehydration with loss of fluid more then 10 % of body weight.

Clinical manifestations

Clinical manifestations of cholera, caused by classic vibrion and vibrion El-Tor are similar.

In mild course (dehydration of the first degree). The loss of fluid is till 3 % of body weight. In majority patients stool may be till 10 times in a day, scanty. In one-third of the patients vomiting may occur 1-2 times. Thirst, light dizziness, weakness trouble the patients. Their state is satisfactory. Skin is humid, usual color. The mucous of the mouth is dry. There is no hypothermia. Subfebrile temperature may be in the part of the patients. There are no changes of the pulse and arterial pressure. An insignificant painfulment occurs due to palpation of the stomach. The changes of the blood are not typical. There is no blood’s condensation, change it’s pH and electrolytes.

After corresponding therapy a vomiting, dizziness, weakness disappear at the first day. The stool become normal on the 2-3 day of the treatment.

A cyanosis of lips and extremities is observed. The skin is cold and shriveled. The turgor decreases. The face is pinched, eyes are deeply sunken in the orbits. In a third of the patients a symptom of “black eyeglasses” is observed (Fig.6). The mucous of the mouth cavity is dry. The lips are dry too. Tongue is dry and covered. A voice becomes hoarse. The cramps are often of long duration, with tonic character. Cramps are accompanied with pain. The cramps of the trunk muscles and diaphragm are not observed. The temperature is 35.7-35.5 ºC. The pulse is 120-130 in a minute, weak. The arterial pressure is low 80/50 mm. Sometimes the breathlessness occurs. Renal failure is manifested by olyguria, in 25 % – by anuria. There are erythrocytosis, leucocytosis, neutrophylosis with the shift of the formula to the left, lymphopenia, uneosinophilia. The concentration of hemoglobin increases. Protein and leukocytes are observed in urine. Hematocrit is 55-65 L/L in these patients. The relative density of plasma is 1030-1035. There is considerable change of electrolytes. Hypokalemia, hypochlorinemia are expressive.

Extremly severe course (dehydration of the forth degree) or decompensated dehydration. It occurs more rarely than the other clinical variants. The loss of fluid is 10 % of body weight and more.

Untreated patients die. The cause of the death is an acute heart’s failure (at the first three days of the disease) or renal failure (up to 14-16 day).

Diagnosis

Differential diagnosis

Differential diagnostics of cholera is performed with toxical food-borne infections, esherichiosis, rotaviral gastroenteritis. In some untypical cases of cholera, especially in obliterated course of the disease it is necessary to perform differentiation of gastrointestinal form of salmonellosis, gastroenterocolitic variant of acute shigellosis, poisoning with mashrooms, organic and inorganic chemical remedies.

Treatment

http://infectiousdiseases.about.com/od/diseasesbyname/a/cholera.htm

For prevention of side reactions of polyionic solutions preliminary warm up to 38 – 40 °С, at the first hours of treatment infuse Prednisolon 0,5 gr/kg per day. At infusion there is plenty of solution Trisol the metabolic alkalosis and hyperkalemia can be developed. In these cases infusion therapy is continued with solution Disol.

In case of I-II stages dehydration (liquid loss up to 6 % of body weight) and more severe dehydration is managed by intravenous injection of saline solutions, at absence of vomiting recommend to apply peroral indication of Glucosani in tablets or Rehydroni in packages 18,9 gr: the content of 1 package dissolve in 1 L of boiled water and drink small portions.

Water-salt therapy should be over after appearance of excrements of normal character and at prevalence of quantity of urine over quantity of excrements in the last 6-12 hours.

Panangin or Asparcam during 1 mounth are indicated during early reconvalescence.

Rehydration therapy is directed at restoration of the water-salt equilibrium and is used in gastrointestinal forms of intestinal infections attended by incoercible vomiting, frequent stools (profuse diarrhea), dehydration of the body and accordingly decreasing volume of circulating blood (hypovolaemia), and development of hypovolaemic shock.

The amount of repleted salts, their composition and the way of administration depend on the rate and degree of dehydration and the character of the water-salt disbalance. Four degrees of dehydration are differentiated.

Dehydration, degree I. The patient loses water in the amount of 1-3 per cent of body weight. The patient develops moderate thirst, dryness of the mucosa, and moderate fatigue; stools are semiliquid or watery, 3-10 times a day; vomiting is rare.

Dehydration, degree II. The loss of liquid is 4-6 per cent of body weight. Stools are ample, watery, or resembling rice water, 10-20 times a day; vomiting is frequent (5-Ю times). The patient develops thirst, the skin and mucosa are dry; the lips, fingers and feet are cyanotic; fatigue is marked. Muscular cramping in the calves, wrists, and feet; signs of blood thickening develop; tachycardia, hypotension and oliguria are seen.

Dehydration, degree III. The loss of liquid is 7-9 рьг cent of body weight. Stools are frequent and ample; vomiting and cramping of limb muscles are seen; the skin and mucosa are dry, washerwoman’s hands symptom develops, hypotension is pronounced; oliguria or even anuria develops.

Dehydration, degree IY (the algid form). The liquid loss is 10 per cent of body weight. The disease begins acutely. Diarrhoea and vomiting discontinue at the beginning of the disease. The body temperature falls to 35-35.5 °С, peripheral pulse and arterial pressure are absent; anuria and aphonia develop. Cyanosis is intensive, the muscles are cramping, the facies are pinched, the eyes and the cheeks are retracted.

In I and II degree dehydration the patient is given gastric lavage and then one of the following solutions (to drink in small portions):

Glucose-salt mixture (3.5 gm of sodium chloride, 2.5 g m of sodium hydrocarbonate, 1.5 gm of potassium chloride, and 20 gm of glucose dissolved ex tempore in 1 litre of drinking water); a solution containing 4 gm of sodium hydrocarbonate, 5 gm of sodium chloride, and 1 g of potassium chloride; a solution containing 2.6 gm of sodium acetate, 1 g of sodium hydrocarbonate, 6.2 gm of sodium chloride, and 0.3 g m of potassium chloride; or Locke-Ringer solution containing glucose or sweet tea. If vomiting continues, the liquid should be administered through a nasogastric tube.

In II and III degree dehydration, and especially degree IV, the patient should be given intravenously polyion buffer solutions preheated to 38-40 °С. In addition to the mentioned solutions, used also are solutions containing 2 gm of sodium acetate, 5 gm of sodium chloride, 1.0 gm of potassium chloride, or a solution containing 3.6 g m of sodium acetate, 4.75 gm of sodium chloride, and 1.5 gm of potassium chloride, or a solution containing 3.3 gm of sodium lactate, 4.75 gm of sodium chloride, and 1.5 gm of potassium chloride. Treatment includes two states: primary rehydration (repletion of the liquid lost before rehydration therapy is started) and compensatory (replenishment of the liquid lost during treatment).

In III degree dehydration the solution is given intravenously at a rate of 100 ml/min. In IV degree dehydration, and if hypovolaemic shock develops, one of the specified solutions is infused at a rate of 100-120 mL/min, 5-7 litres during 60-90 minutes. After the patient’s condition is no longer critical, the second stage of treatment begins. The solution is now infused by drip at a rate of 100-150 drops per minute with a gradual reduction of the rate to 60 and then 20-10 drops per minute. Liquid infusion can be suspended depending on the degree of improvement of the patient’s condition and normalization of the water-salt metabolism. If necessary, the glucose-salt solutions are given per os, by small portions at short time intervals.

Salt solutions, especially their large volumes, should be administered under constant laboratory control of the water-electrolyte metabolism, blood counts, and diuresis.

Botulism

http://www.nlm.nih.gov/medlineplus/botulism.html

Botulism also known as botulinus intoxication is a rare but serious paralytic illness caused by botulinum toxin, which is produced by the bacterium Clostridium botulinum under anaerobic conditions.

The toxin enters the body in one of three ways: by colonization of the digestive tract by the bacterium in children (infant botulism) or adults (adult intestinal toxemia), by ingestion of toxin from foods (foodborne botulism) or by contamination of a wound by the bacterium (wound botulism).

All forms lead to paralysis that typically starts with the muscles of the face and then spreads towards the limbs.In severe forms, it leads to paralysis of the breathing muscles and causes respiratory failure. In view of this life-threatening complication, all suspected cases of botulism are treated as medical emergencies, and public health officials are usually involved to prevent further cases from the same source.

Botulism can be prevented by killing the spores by cooking at 121 °C (250 °F) for 3 minutes or providing conditions that prevent the spores from growing. Additional precautions for infants include not feeding them honey.

Clinical features

The muscle weakness of botulism characteristically starts in the muscles supplied by the cranial nerves. A group of twelve nerves controls eye movements, the facial muscles and the muscles controlling chewing and swallowing. Double vision, drooping of both eyelids, loss of facial expression and swallowing problems may therefore occur, as well as difficulty with talking. The weakness then spreads to the arms (starting in the shoulders and proceeding to the forearms) and legs (again from the thighs down to the feet). Severe botulism leads to reduced movement of the muscles of respiration, and hence problems with gas exchange. This may be experienced as dyspnea (difficulty breathing), but when severe can lead to respiratory failure, due to the buildup of unexhaled carbon dioxide and its resultant depressant effect on the brain. This may lead to coma and eventually death if untreated.

Ptosis

In addition to affecting the voluntary muscles, it can also cause disruptions in the autonomic nervous system. This is experienced as a dry mouth and throat (due to decreased production of saliva), postural hypotension (decreased blood pressure on standing, with resultant lightheadedness and risk of blackouts), and eventually constipation (due to decreased peristalsis). Some of the toxins (B and E) also precipitate nausea and vomiting.

Clinicians frequently think of the symptoms of botulism in terms of a classic triad: bulbar palsy and descending paralysis, lack of fever, and clear senses and mental status (“clear sensorium”).

Dryness of tongue

Squint, midriasis, anizocory

Mode of acquisition

Four main modes of entry for the toxin are known. The most common form in Western countries is infant botulism. This occurs in small children who are colonized with the bacterium during the early stages of their life. The bacterium then releases the toxin into the intestine, which is absorbed into the bloodstream. While the consumption of honey during the first year of life has been identified as a risk factor for infant botulism, it is a factor in a fifth of all cases. The adult form of infant botulism is termed adult intestinal toxemia, and is exceedingly rare.

Foodborne botulism results from contaminated foodstuffs in which C. botulinum spores have been allowed to germinate in anaerobic conditions. This typically occurs in home-canned food substances and fermented uncooked dishes. Given that multiple people often consume food from the same source, it is common for more than a single person to be affected simultaneously. It takes 3–5 days for the symptoms to become apparent.

Wound botulism results from the contamination of a wound with the bacteria, which then secrete the toxin into the bloodstream. This has become more common in intravenous drug users since the 1990s, especially people using black tar heroin and those injecting heroin into the skin rather than the veins.

Isolated cases of botulism have been described after inhalation by laboratory workers and after cosmetic use of inappropriate strengths of Botox.

Infant botulism

Infant botulism was first recognized in 1976, and is the most common form of botulism in the United States. There are 80 – 100 diagnosed cases of infant botulism in the United States each year. Infants are susceptible to infant botulism in the first year of life, with more than 90 % of cases occurring in infants younger than six months. Infant botulism results from the ingestion of the C. botulinum spores, and subsequent colonization of the small intestine. The infant gut may be colonized when the composition of the intestinal microflora (normal flora) is insufficient to competitively inhibit the growth of C. botulinum. Medical science does not yet completely understand all factors that make an infant susceptible to C. botulinum colonization. The growth of the spores releases botulinum toxin, which is then absorbed into the bloodstream and taken throughout the body, causing paralysis by blocking the release of acetylcholine at the neuromuscular junction. Typical symptoms of infant botulism include constipation, lethargy, weakness, difficulty feeding and an altered cry, often progressing to a complete descending flaccid paralysis. Although constipation is usually the first symptom of infant botulism, it is commonly overlooked.

Honey is the only known dietary reservoir of C. botulinum spores linked to infant botulism. For this reason honey should not be fed to infants less than one year of age. Due to the success of this public health message, fewer than 5 % of recent infant botulism cases have been exposed to honey. The remaining 95 % of infant botulism cases are thought to have acquired the spores from the natural environment. Clostridium botulinum is a ubiquitous soil-dwelling bacterium. Many infant botulism patients have been demonstrated to live near a construction site or an area of soil disturbance.

Infant botulism has been reported in 49 of 50 US states, and cases have been recognized in 26 countries on five continents.

Complications

Infant botulism has no long-term side effects, but can be complicated by nosocomial adverse events. The case fatality rate is less than 1% for hospitalized infants with botulism.

Botulism can result in death due to respiratory failure. However, in the past 50 years, the proportion of patients with botulism who die has fallen from about 50 % to 8 % due to improved supportive care. A patient with severe botulism may require a breathing machine as well as intensive medical and nursing care for several months. Patients who survive an episode of botulism poisoning may have fatigue and shortness of breath for years and long-term therapy may be needed to aid their recovery.

Mechanism

C. botulinum is an anaerobic, Gram positive, spore-forming rod. Botulin toxin is one of the most powerful known toxins: about one microgram is lethal to humans. It acts by blocking nerve function and leads to respiratory and musculoskeletal paralysis.

In all cases illness is caused by the toxin made by C. botulinum, not by the bacterium itself. The pattern of damage occurs because the toxin affects nerves that are firing more often. Specifically, the toxin acts by blocking the production or release of acetylcholine at synapses and neuromuscular junctions. Death occurs due to respiratory failure.

Diagnosis

For infant botulism, diagnosis should be made on clinical grounds. Confirmation of the diagnosis is made by testing of a stool or enema specimen with the mouse bioassay.

Physicians may consider diagnosing botulism if the patient’s history and physical examination suggest botulism. However, these clues are ofteot enough to allow a diagnosis. Other diseases such as Guillain-Barré syndrome, stroke, and myasthenia gravis can appear similar to botulism, and special tests may be needed to exclude these other conditions. These tests may include a brain scan, cerebrospinal fluid examination, nerve conduction test (electromyography, or EMG), and an edrophonium chloride (Tensilon) test for myasthenia gravis. A definite diagnosis can be made if botulinum toxin is identified in the food, stomach or intestinal contents, vomit or feces. The toxin is occasionally found in the blood in peracute cases. Botulinum toxin can be detected by a variety of techniques, including enzyme-linked immunosorbent assays (ELISAs), electrochemiluminescent (ECL) tests and mouse inoculation or feeding trials. The toxins can be typed with neutralization tests in mice. In toxicoinfectious botulism, the organism can be cultured from tissues. On egg yolk medium, toxin-producing colonies usually display surface iridescence that extends beyond the colony.

In cattle, the symptoms may include drooling, restlessness, uncoordination, urine retention, dysphagia, and sternal recumbency. Laterally recumbent animals are usually very close to death. In sheep, the symptoms may include drooling, a serous nasal discharge, stiffness, and incoordination. Abdominal respiration may be observed and the tail may switch on the side. As the disease progresses, the limbs may become paralyzed and death may occur.

The clinical signs in horses are similar to cattle. The muscle paralysis is progressive; it usually begins at the hindquarters and gradually moves to the front limbs, neck, and head. Death generally occurs 24 to 72 hours after initial symptoms and results from respiratory paralysis. Some foals are found dead without other clinical signs.

Pigs are relatively resistant to botulism. Reported symptoms include anorexia, refusal to drink, vomiting, pupillary dilation, and muscle paralysis.

In poultry and wild birds, flaccid paralysis is usually seen in the legs, wings, neck and eyelids. Broiler chickens with the toxicoinfectious form may also have diarrhea with excess urates.

Prevention

Although the botulinum toxin is destroyed by thorough cooking over the course of a few minutes, the spore itself is not killed by the temperatures reached with normal sea-level-pressure boiling, leaving it free to grow and again produce the toxin when conditions are right.

A recommended prevention measure for infant botulism is to avoid feeding honey to infants less than 12 months of age.

While commercially canned goods are required to undergo a “botulinum cook” at 121 °C (250 °F) for 3 minutes, and so rarely cause botulism, there have beeotable exceptions such as the 1978 Alaskan salmon outbreak and the 2007 Castleberry’s Food Company outbreak. Foodborne botulism has more frequently been from home-canned foods with low acid content, such as carrot juice, asparagus, green beans, beets, and corn. However, outbreaks of botulism have resulted from more unusual sources. In July, 2002, fourteen Alaskans ate muktuk (whale meat) from a beached whale, and eight of them developed symptoms of botulism, two of them requiring mechanical ventilation. Other sources of infection include garlic or herbs stored covered in oil without acidification, chilli peppers, improperly handled baked potatoes wrapped in aluminium foil, tomatoes, and home-canned or fermented fish. Persons who do home canning should follow strict hygienic procedures to reduce contamination of foods. Oils infused with garlic or herbs should be acidified and refrigerated. Potatoes which have been baked while wrapped in aluminum foil should be kept hot until served or refrigerated. Because the botulism toxin is destroyed by high temperatures, home-canned foods are best boiled for 20 minutes before eating. Metal cans containing food in which bacteria, possibly botulinum, are growing may bulge outwards due to gas production from bacterial growth; such cans should be discarded. Any container of food which has been heat-treated and then assumed to be airtight which shows signs of not being so, e.g., metal cans with pinprick holes from rust or mechanical damage, should also be discarded.

Wound botulism can be prevented by promptly seeking medical care for infected wounds, and by avoiding punctures by unsterile things such as needles used for street drug injections. It is currently being researched at USAMRIID under BSL-4.

Treatment

http://www.mayoclinic.com/health/botulism/DS00657/DSECTION=treatments-and-drugs

Most infant botulism patients require supportive care in a hospital setting. The only drug currently available to treat infant botulism is Botulism Immune Globulin Intravenous-Human (BIG-IV or BabyBIG). BabyBIG was developed by the Infant Botulism Treatment and Prevention Program at the California Department of Public Health.

The respiratory failure and paralysis that occur with severe botulism may require a patient to be on a ventilator for weeks, plus intensive medical and nursing care. After several weeks, the paralysis slowly improves. If diagnosed early, foodborne and wound botulism can be treated by inducing passive immunity with a horse-derived antitoxin, which blocks the action of toxin circulating in the blood. This can prevent patients from worsening, but recovery still takes many weeks. Physicians may try to remove contaminated food still in the gut by inducing vomiting or by using enemas. Wounds should be treated, usually surgically, to remove the source of the toxin-producing bacteria. Good supportive care in a hospital is the mainstay of therapy for all forms of botulism.

Furthermore each case of food-borne botulism is a potential public health emergency in that it is necessary to identify the source of the outbreak and ensure that all persons who have been exposed to the toxin have been identified, and that no contaminated food remains.

There are two primary Botulinum Antitoxins available for treatment of wound and foodborne botulism. Trivalent (A,B,E) Botulinum Antitoxin is derived from equine sources utilizing whole antibodies (Fab & Fc portions). This antitoxin is available from the local health department via the CDC. The second antitoxin is heptavalent (A, B, C, D, E, F, G) Botulinum Antitoxin which is derived from “despeciated” equine IgG antibodies which have had the Fc portion cleaved off leaving the F(ab)2 portions. This is a less immunogenic antitoxin that is effective against all known strains of botulism where not contraindicated. This is available from the US Army. On 1 June 2006 the US Department of Health and Human Services awarded a $363 million contract with Cangene Corporation for 200,000 doses of Heptavalent Botulinum Antitoxin over five years for delivery into the Strategic National Stockpile beginning in 2007.