View source for Medicine:Alimentary toxic aleukia

{{Infobox medical condition (new)
| name          = <!--{{PAGENAME}} by default-->
| synonym       = Aleukia, ATA
| image         = Alimentary_Toxic_Aleukia.png
| image_size    = 
| alt           = 
| caption       = Stages of Alimentary Toxic Aleukia
| pronounce     = 
| specialty     = <!-- from Wikidata, can be overwritten -->
| symptoms      = Nausea, vomiting, [[Medicine:Diarrhea|diarrhea]], [[Medicine:Leukopenia|leukopenia]] (aleukia), [[Medicine:Bleeding|hemorrhaging]], skin inflammation.<ref name="Lutsky Mor p. "/>
| complications = 
| onset         = 
| duration      = 
| types         = 
| causes        = Intake of [[Biology:Fungus|fungi]]-infested overwintered grain or grain by-products.<ref name="Lutsky Mor p. "/>
| risks         = 
| diagnosis     = 
| differential  = 
| prevention    = 
| treatment     = Excluding various wintered grain products and flour from the diet.
| medication    = 
| prognosis     = 
| frequency     = 
| deaths        = 
}}
'''Alimentary toxic aleukia''' is a [[Chemistry:Mycotoxin|mycotoxin]]-induced condition characterized by nausea, vomiting, [[Medicine:Diarrhea|diarrhea]], [[Medicine:Leukopenia|leukopenia]] (aleukia), [[Medicine:Bleeding|hemorrhaging]], skin inflammation, and sometimes death.<ref name="Lutsky Mor p. ">{{cite journal | last1=Lutsky | first1=I. I. | last2=Mor | first2=N. | title=Alimentary toxic aleukia (septic angina, endemic panmyelotoxicosis, alimentary hemorrhagic aleukia): t-2 toxin-induced intoxication of cats. | journal=The American Journal of Pathology | date=1981 | publisher=American Society for Investigative Pathology | volume=104 | issue=2 | pages=189–191 | pmid=6973281 | pmc=1903757 }}</ref> Alimentary toxic aleukia almost always refers to the human condition associated with presence of T-2 Toxin.<ref name="Lutsky Mor p. "/>

==Signs and symptoms==
Alimentary toxic aleukia manifests in inflammation of the [[Biology:Stomach|gastric]] and [[Biology:Gastrointestinal wall|intestinal mucosa]], a severe progressive [[Medicine:Leukopenia|leukopenia]], [[Medicine:Anemia|anemia]], and an increased [[Erythrocyte sedimentation rate|erythrocyte sedimentation rate]]. Subsequently petechial hemorrhages of both the skin and [[Biology:Mucous membrane|mucosa]] as well as enlarged lymph nodes are seen. Symptoms of the respiratory system include [[Medicine:Bronchopneumonia|bronchopneumonia]], [[Medicine:Pulmonary hemorrhage|pulmonary hemorrhage]]s, [[Medicine:Sepsis|sepsis]], and [[Medicine:Lung abscess|lung abscess]]es. Vomiting, bloody stools, lassitude, and incoordination are also observed.<ref name="Lutsky Mor p. "/> The severity of the disease and its course was determined by the quantity of the [[Biology:Toxin|toxin]] and the various reactive properties of various tissues and organs to the toxin.<ref name="Food and Agriculture Organization of the United Nations"/>

There are four stages of ATA. The first stage is acute intoxication. The [[Medicine:Leukopenia|leukopenia]] stage is the next. The third stage is distinguished by distinct clinical symptoms (anginal-[[Medicine:Bleeding|hemorrhagic]] stage), and the fourth by recovery and possible complications.<ref name="Food and Agriculture Organization of the United Nations">{{cite journal |last1=Efremov |first1=V.V |title=Alimentary Toxic Aleukia: Epidemiology, Etiology, Pathogenenesis, Clinical Manifestations, Therapy. |pages=1–25 |url=https://wedocs.unep.org/bitstream/handle/20.500.11822/22522/Alimentary%20_Aleukia.pdf?sequence=1&isAllowed=y |access-date=1 October 2023 |publisher=Food and Agriculture Organization of the United Nations |location=Moscow}}</ref>

===Stage One===
Local and systemic symptoms can appear immediately or several hours after consuming a meal prepared with the toxic wintered grain. Local symptoms include a bitter taste in the mouth, which leads to a complete loss of taste, [[Biology:Tongue|tongue]] numbness or swelling, a burning sensation in the mouth, and pain when swallowing. If no more hazardous grain was consumed, the foregoing symptoms subsided within 2 or 3 days, but they resurfaced as soon as the patient resumed consumption of this grain. Toxemia manifested as [[Medicine:Weakness|weakness]], malaise, [[Medicine:Rheumatoid arthritis|rheumatic]]-like pain, hyperhidrosis, a condition similar to [[Medicine:Alcohol intoxication|alcohol intoxication]], and [[Medicine:Insomnia|insomnia]]. These symptoms typically go away in 3 to 5 days.<ref name="Food and Agriculture Organization of the United Nations"/>

There were isolated cases of acute food poisoning resulting in acute [[Medicine:Esophagitis|esophagitis]], [[Medicine:Gastritis|gastritis]], or [[Medicine:Gastroenteritis|gastroenteritis]], with hypersalivation, nausea, vomiting, esophageal and [[Medicine:Abdominal pain|stomach pain]], [[Medicine:Diarrhea|diarrhea]], and fevers of up to 39 degrees. [[Medicine:Dizziness|Giddiness]], headache, [[Medicine:Mydriasis|mydriasis]], [[Medicine:Tachycardia|tachycardia]], [[Medicine:Cyanosis|cyanosis]], limb coldness, and [[Medicine:Convulsion|convulsion]]s were also reported. There were also [[Medicine:Bleeding diathesis|hemorrhagic diathesis]] with cutaneous and [[Biology:Mucous membrane|mucosal]] hemorrhages and [[Medicine:Nosebleed|epistaxis]]. In such circumstances, the blood count can indicate [[Biology:Haematopoiesis|hematopoiesis]] alterations as quickly as 1-4 days; this was followed by [[Medicine:Neutropenia|neutropenia]] and relative lymphocytosis, [[Medicine:Thrombocytopenia|thrombocytopenia]], and some [[Erythrocyte sedimentation rate|erythrocyte sedimentation rate]] acceleration.<ref name="Food and Agriculture Organization of the United Nations"/>

===Stage Two===
With the subsequent ingesting of the toxic grain, the disease advances and enters the second stage within a few days. Because there is no habituation to the harmful substance, local symptoms may reoccur. The duration of the ATA leukopenia stage could vary from 2-3 weeks to 6-8 weeks and even 3-4 months. Clinically, the [[Medicine:Leukopenia|leukopenia]] stage manifests as symptoms of the [[Biology:Central nervous system|central]] and vegetative nervous systems. Patients reported [[Medicine:Fatigue|fatigue]], [[Philosophy:Apathy|apathy]], [[Medicine:Vertigo|vertigo]], headache, and [[Medicine:Insomnia|poor sleep]]. The patients' skin would appear pale, and dry, and the symptoms of late dermographism [[Medicine:Mydriasis|mydriasis]] would be clearly visible. The patients showed a petechial rash towards the end of the [[Medicine:Leukopenia|leukopenia]] stage. The petechial patches were initially quite little, but as the disease advanced, they grew in size. When the [[Medicine:Leukopenia|leukopenia]] stage was treated promptly and adequately, it was often followed by recovery.<ref name="Food and Agriculture Organization of the United Nations"/>

===Stage Three===
Acute symptoms such as rash, [[Medicine:Bleeding|hemorrhages]], [[Biology:Necrosis|necrotic]] [[Medicine:Angina|angina]], [[Medicine:Fever|high temperature]], and [[Medicine:Tachycardia|tachycardia]] mark the third ATA stage. The [[Biology:White blood cell|leukocyte]] count continues to fall. [[Medicine:Bleeding time|Bleeding time]] increases, and the coagulability of the blood is delayed. [[Medicine:Bleeding|Hemorrhages]] occur in the nose, [[Biology:Pharynx|pharynx]], [[Biology:Esophagus|esophagus]], gut, kidney, [[Biology:Bladder|bladder]], and [[Biology:Uterus|uterus]]. [[Medicine:Bleeding|Hemorrhages]] can be severe and difficult to control, resulting in significant blood loss and even death. Patients develop [[Medicine:Angina|angina]] several days following the formation of the petechial rash, which in severe cases might be necrotic or gangrenous. The tonsils completely decomposed, followed by acute edema of the [[Medicine:Laryngeal vestibule|laryngeal vestibule]] and blockage within 3-8 days with [[Biology:Necrosis|necrotic]] masses and [[Medicine:Thrombus|blood clots]]. Asphyxia and [[Medicine:Aphonia|aphonia]] ensued, and many people died as a result. The [[Medicine:Gangrene|gangrenous]] process progressed to the [[Medicine:Soft palate|soft palate]], gums, tongue, lips, cheeks, and nasal cavity, resulting in tooth loss and cheek perforation. These symptoms were particularly prevalent in individuals who had an imbalanced diet and in children. Severe [[Medicine:Angina|angina]]l symptoms were followed by an increase in [[Medicine:Bleeding diathesis|hemorrhagic diathesis]]. Acute [[Medicine:Hepatitis|hepatitis]] typically manifests itself during the third ATA stage. The [[Biology:Liver|liver]] would become slightly enlarged, while the [[Biology:Spleen|spleen]] would remain normal. There was microhematuria and, on rare occasions, [[Medicine:Hematuria|hematuria]]. Even in the most severe cases, significant improvements and even recovery within 1-2 weeks was feasible. Heart paralysis, uncontrollable [[Medicine:Bleeding|hemorrhages]], suffocation, [[Medicine:Pneumonia|pneumonia]] with pulmonary abscesses, and [[Medicine:Gangrene|gangrene]] all contributed to death.<ref name="Food and Agriculture Organization of the United Nations"/>

===Stage Four===
When [[Medicine:Pathogenesis|pathogenetic]] therapy was administered, the condition advanced to the fourth stage, which lasted 10-14 days. The [[Biology:Necrosis|necrotic]] fool began to mend and [[Medicine:Bleeding|hemorrhages]] stopped during this pealed; a reduction of fever showed recovery from acute toxemia. However, lingering toxic symptoms ([[Medicine:Tachycardia|tachycardia]], [[Medicine:Hypotension|hypotension]], apical systolic murmur, left heart dilatation, dyspnea, [[Medicine:Weakness|weakness]], [[Medicine:Vertigo|vertigo]], [[Medicine:Gastritis|gastritis]], [[Medicine:Gastroenteritis|gastroenteritis]], [[Medicine:Hepatitis|hepatitis]], [[Biology:Central nervous system|central]] and vegetative nervous system problems) persisted for an extended period of time.<ref name="Food and Agriculture Organization of the United Nations"/>

==Treatment==
At the early stages of the condition, therapeutic measures include excluding various wintered grain products and flour from the diet and monitoring [[Biology:Red blood cell|erythrocyte]], [[Biology:Platelet|platelet]], and [[Biology:White blood cell|leukocyte]] differential counts. In the second stage, therapeutic interventions include balanced nutrition, which includes biologically beneficial [[Biology:Protein|protein]]s and [[Chemistry:Vitamin|Vitamin]]s such as [[Chemistry:Ascorbic acid|ascorbic acid]], [[Physics:Thiamine|thiamine]], [[Biology:Riboflavin|riboflavin]], [[Chemistry:Niacin|niacin]], [[Chemistry:B vitamins|vitamin B]], [[Chemistry:Folate|folacin]], and [[Chemistry:Vitamin E|vitamin E]].<ref name="Food and Agriculture Organization of the United Nations"/>

When the condition reaches the third stage, the patient is immediately hospitalized and placed on a balanced diet. Early prescription or large doses of [[Chemistry:Sulfamide|sulfamide]] compounds and adequate [[Chemistry:Antibiotic|antibiotic]]s were required, as well as the use of general and [[Biology:Haematopoiesis|hemopoiesis]]-stimulated [[Medicine:Blood transfusion|blood transfusion]] and [[Unsolved:Autologous blood therapy|autohemotherapy]], the administration of [[Medicine:Antihemorrhagic|hemostatic]], detoxicating, and cardiovascular activity-stimulating agents, and the local treatment of [[Biology:Necrosis|necrotic]] foci.<ref name="Food and Agriculture Organization of the United Nations"/>

In the fourth stage, medical treatments would be focused on increasing the body's response capacity through general bracing and [[Biology:Haematopoiesis|hemopoiesis]] stimulation, as well as eradicating toxic residual effects with detoxication medications.<ref name="Food and Agriculture Organization of the United Nations"/>

==History==
Alimentary toxic aleukia was first characterized in the early 20th century after affecting a large population in the Orenburg Oblast of the former USSR in 1933 and during [[Social:World War II|World War II]]. The sick people had eaten overwintered grain colonized with ''[[Biology:Fusarium sporotrichioides|Fusarium sporotrichioides]]'' and ''Fusarium poae''.<ref>{{cite journal | pmc= 164220 | pmid=12857779 | volume=16 | issue=3 | title=Mycotoxins | date=July 2003 | journal=Clin. Microbiol. Rev. | pages=497–516 | last1 = Bennett | first1 = JW | last2 = Klich | first2 = M | doi=10.1128/cmr.16.3.497-516.2003}}</ref>

==References==
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[[Category:Blood disorders]]

{{Sourceattribution|Alimentary toxic aleukia}}