Alimentary toxic aleukia is a severe food intoxication caused by mycotoxins of fungi of the genus Fusarium. The specific effect of the toxin is the defeat of lymphoid tissue and bone marrow. The main manifestations of the disease are necrotic angina and hemorrhagic syndrome. Diagnosis consists in detecting the pathogen during bacteriological examination of the patient’s blood and tissues, no less important is the careful collection of anamnesis, the presence of characteristic changes in the tonsils and leukopenia in blood test. Treatment consists of detoxification, systemic and local antibacterial therapy, may include transfusion of blood components.
General information
Alimentary toxic aleukia, also known as septic, alimentary-hemorrhagic angina and acute alimentary mycotoxicosis, is a severe poisoning caused by the toxin of fusarium fungi. The path of infection is food, most often associated with the consumption of products from overwintered grain containing fungal spores. The pathology was first described in 1932 during an epidemic in Kazakhstan; it is found all over the globe. It was found that residents of agricultural areas are most susceptible to infection, usually an increase in the number of cases is observed in the period from April to June. A sick person is not contagious to others.
Causes
The causative agents of the disease are fungi of the genus Fusarium, which produce the toxin poin, which causes local manifestations in the form of necrosis and has a tropicity to hematopoietic and lymphoid tissues. The source of infection is grain crops, which served as a breeding ground for reproduction and accumulation of poin during wintering. Such agricultural plants include millet, buckwheat, wheat, rye, oats and barley. Favorable conditions for the growth of the fungus are high humidity, the presence of oxygen and heat. In the cold season, fungi turn into spores and survive the winter, and after the onset of spring they begin to produce points again.
Risk factors for the outbreak of the disease are considered warm winter and early spring, as well as high humidity and other violations of the rules of grain storage. The toxin does not break down during heat treatment, fermentation, and is able to retain its properties for up to five years, especially at a storage temperature range from -1 ° C to +5 ° C. Patients with immunosuppression (HIV infection, long-term therapy with corticosteroids, immunosuppressants), persons after splenectomy, children, agricultural workers, food industry workers, public catering are considered risk groups for morbidity.
Pathogenesis
After the poin hits the mucous membranes, a local reaction occurs associated with necrotic tissue changes due to extensive inflammation. Through the wound surface, the toxin is intensively absorbed into the blood, spreads throughout the body, showing tropicity to the myeloid (red stagnant brain) and later to the lymphoid tissue. Under the influence of poin, hematopoiesis is suppressed, inflammatory changes occur in the thymus, spleen, lymph nodes, Peyer’s plaques and appendix. Gradually, there is a decrease in the number of erythrocytes, monocytes, granulocytes, platelets, precursors of T-lymphocytes, B-lymphocytes and NK cells, as well as macrophages, dendritic cells. Hemorrhagic changes occur in parenchymal organs, skin, septic condition develops. Immunity after the disease is persistent, but its duration has not been studied.
Classification
In the clinic of alimentary mycotoxicosis, two variants of the course are distinguished, which are directly dependent on the amount of grain product eaten, the toxigenicity of the strain, the concentration of the toxin in the food product and the immune competence of the body of the patient:
- Lightning fast. It is characterized by a rapid increase in clinical manifestations and a fatal outcome during the first day of the disease due to a developed DIC syndrome or sepsis.
- Typical. It lasts about 3-4 weeks, is characterized by a gradual increase in the severity of the condition and pronounced stages. It includes toxic, leukopenic and anginous-hemorrhagic stages.
Symptoms of alimentary toxic aleukia
The incubation period is from 2 to 6 weeks, with the use of a large number of products from infected grain (more than 500 g), symptoms appear after a few days. The first signs of poisoning are nausea, vomiting, liquid watery stools, weakness, decreased performance and fatigue. The described manifestations last about 3 days, followed by a period of leukopenia. Clinically, this condition reveals itself as an increase in weakness, malaise, drowsiness (this stage usually lasts 2-3, less often 6-8 weeks).
In the future, with the aggravation of the toxic effect, the anginous-hemorrhagic stage occurs. Patients complain of high rises in body temperature (more than 39 ° C), terrific chills, note the appearance of spot hemorrhages (petechiae) on the body, less often – ecchymoses; gingival and nasal bleeding. At the same time, severe pain occurs when swallowing, unpleasant putrid breath, dirty-gray plaque on the tonsils, in the oral cavity, larynx and pharynx. With the progression of the disease, phlegmons and skin abscess, fiber and internal organs are formed.
Complications
Complications usually manifest during the lightning-fast course of food mycotoxicosis or in the anginous-hemorrhagic period of a typical variant of the disease. The most common of these are pneumonia, bronchitis, lung abscess, soft tissue phlegmons and osteomyelitis. In conditions of increasing immunosuppression, these conditions can lead to sepsis. In some cases, there is the appearance of necrotic changes in the distal extremities. Deficiency of the blood coagulation system, damage to parenchymal organs (kidneys, liver, spleen) lead to the development of DIC syndrome with a characteristic clinic of massive uncupable bleeding.
Diagnostics
If alaikia of alimentary toxic genesis is suspected, it is mandatory to consult an infectious disease specialist, an otorhinolaryngologist, a pulmonologist; after the appearance of skin ulcers and internal organs, a surgeon. In order to identify the pathogen, assess the nature and severity of changes, laboratory and instrumental examinations are performed:
- Blood test. In the general blood test, pronounced leukopenia, thrombocytopenia, anemia, acceleration of ESR are observed. Biochemical indicators reflect an increase in the activity of AST, ALT, creatinine, urea.
- Identification of infectious agents. Isolating a fungus from human tissues and blood is a time-consuming and expensive process. Bacterial analysis is performed by seeding the material on nutrient media. The detection of the toxin in the grain is carried out using a biological test (feeding laboratory pigeons with suspicious grain, skin test on rabbits), grain chromatography.
- Endoscopy of ENT organs. When examining the pharynx – pharyngoscopy – signs of catarrhal, necrotic or gangrenous angina are detected. Typical raids are dirty gray or brown, passing from the tonsils to the mucous membrane of the larynx, pharynx, oral cavity; bleeding of the mucous membrane of the nose and throat, the formation of necrosis.
When signs of pneumonia appear, chest radiography is performed; ultrasound of the abdominal cavity, pelvis, retroperitoneal space, lymph nodes is used for the purpose of differential diagnosis. Differential diagnosis is carried out with diphtheria, sepsis, systemic mycoses, agranulocytosis, Simanovsky-Plaut-Vincent’s angina, poisoning with heavy metals, radioactive substances.
Treatment of alimentary toxic aleukia
Therapeutic measures begin with the removal of poisoned foods from food, gastric lavage and a siphon enema (or laxative). It is recommended to exclude alcohol, seasonings, fatty, fried, cereal products from the diet, adhere to frequent fractional nutrition, serve food at room temperature (in order to avoid additional injury to the mucous membranes). It is necessary to monitor the drinking regime, while it is preferable to use water or non-acidic juices. After each meal, it is recommended to rinse the mouth with antiseptic solutions (chlorhexidine, furacilin, calendula, sage, chamomile).
Treatment of alimentary toxic aleukia is usually stationary, includes detoxification therapy (glucose-salt solutions) and taking broad-spectrum antibiotics (penicillins, cephalosporins). With a prolonged course of pathology, it may be necessary to replace the loss of blood components: transfusion of erythrocyte, platelet mass, leukocyte concentrate is carried out. There is evidence of a positive effect of the colony-stimulating factor on the course, severity and outcome of the disease. During treatment, it is recommended to reduce the doses of immunosuppressive drugs or cancel them if possible. When localized or spilled purulent processes appear, they are opened and drained, local antibacterial agents (ointments, suspensions) are used.
Prognosis and prevention
With an uncomplicated course, the disease lasts approximately 3-4 weeks. With timely access to medical care, withdrawal of contaminated products from use, manifestations of mycotoxicosis are prone to self-disappearance. With the appearance of hemorrhagic syndrome and necrotic changes in the tonsils, the proportion of deaths is 50-80%. However, for the occurrence of life-threatening conditions, it takes about two to three months of constant consumption of an infected cereal product, even against the background of obvious malaise. Timely hospitalization and thorough epidemiological investigation reduces the risk of death and complications.
Specific prevention (vaccine) has not been developed at this stage of medical development. In order to prevent infection by sanitary supervision bodies, periodic inspections of grain and explanatory work with the population are carried out. The sale and purchase of overwintered grain for the food needs of people and animals is prohibited (delivery to distilleries is allowed). In the territory where sporadic cases of toxic aleukia have been recorded, grain products, raw materials from them are subject to disposal; the population should be examined for leukopenia.
