Differential diagnosis of poliomyelitis and botulism
Poliomyelitis has a number of characteristic neurological manifestations that are important to distinguish from botulism.
- Early manifestations: vomiting, severe weakness, drowsiness, pain along nerve trunks, sometimes impaired consciousness.
- Neurological status: the facial nerve is affected, bulbar syndrome develops (swallowing and speech disorders, dysarthria). Respiratory disorders are observed in some patients.
- Additional signs: meningeal symptoms and back pain are possible, whereas ophthalmoplegic syndrome is atypical.
Important distinction: in poliomyelitis, unlike botulism, there is profuse secretion of mucus and saliva. To confirm the diagnosis, the virus is isolated in cell culture and serological methods (CFT with paired sera) are used.
Diagnosis of encephalitis
The group of encephalitides includes tick-borne, Japanese, spring-summer, West Nile fever, and enteroviral infections (Coxsackie viruses, ECHO).
Diagnosis is based on the following criteria:
- Epidemiological history: visiting wooded areas in spring and summer, tick bites.
- Onset of the disease: acute, with fever, severe headache, and vomiting.
- Symptomatology: hyperesthesia (auditory, visual, olfactory), meningeal signs, cranial nerve involvement (IX–XII pairs), bulbar disorders, and the development of flaccid asymmetrical paralyses.
- State of consciousness: may be depressed up to cerebral coma.
Laboratory confirmation of the diagnosis is achieved by isolating the virus from blood or cerebrospinal fluid (CSF) using bioassays in mice, as well as serological studies (CFT, IHA, ELISA) of paired sera at intervals of several weeks.
Specific therapy for botulism
The mainstay of botulism treatment is detoxification. Specific therapy aims to neutralize freely circulating toxin and should be initiated as early as possible.
For this purpose, botulinum equine antitoxin serum is used, which is available for three types of toxin:
- Type A: 10,000 IU
- Type E: 10,000 IU
- Type B: 5,000 IU
If the toxin type is unknown, a mixture of all three monovalent sera is administered in the specified doses. When the type is established, only the corresponding serum is used.
Amebiasis: causative agent and epidemiology
Amebiasis (amebic dysentery) is a protozoan infection caused by Entamoeba histolytica. It can occur in an intestinal form (ulcerative colitis) or extraintestinal form (formation of abscesses). In endemic regions, up to 90% of cases are asymptomatic carriage.
The causative agent exists in two main forms:
- Cysts: quadrinucleate, highly resistant in the external environment (up to 8 months in water), but killed by drying.
- Trophozoites (vegetative forms): uninucleate, rapidly die outside the body. They are subdivided into non-pathogenic (precystic and luminal) and pathogenic (large vegetative and tissue) forms. Pathogenic forms are motile and produce proteolytic enzymes.
The source of infection is humans. The transmission mechanism is fecal-oral, predominantly foodborne (via greens and vegetables). Men are 10 times more likely to develop amebic liver abscess than women.
Briefly: answers to topical questions
What is the mechanism of action of botulinum toxin at the neuromuscular junction?
The mechanism of action of botulinum toxin involves blocking the release of acetylcholine from nerve endings of the presynaptic membrane into the synaptic cleft. This prevents muscle contraction and leads to paresis and paralysis of various muscle groups, including the respiratory muscles. Botulinum toxin binds to receptors on the presynaptic membrane of motor neurons of the peripheral nervous system, causes proteolysis of proteins inside the neuron, and inhibits acetylcholine secretion.
What drugs are used for etiotropic therapy of amebiasis?
Amebicidal drugs are used to treat amebiasis:
- Luminal amebicides: diloxanide furoate, diiodohydroxyquin, paromomycin, etofamide. Indications: non-invasive forms of E. histolytica, asymptomatic intestinal amebiasis; following treatment with tissue amebicides, for the eradication of E. histolytica colonization.
- Systemic tissue amebicides (5-nitroimidazoles): metronidazole, tinidazole, ornidazole. Indications: invasive forms of E. histolytica, intestinal amebiasis, extraintestinal amebiasis, abscess of any localization.
What extraintestinal forms of amebiasis exist besides liver abscess?
In addition to liver abscess, the following forms of extraintestinal amebiasis exist:
- Amebic hepatitis
- Lung abscess
- Amebic pleuropneumonia
- Brain abscess (left hemisphere is more commonly affected)
- Cutaneous amebiasis
- Urogenital amebiasis (rarely encountered)
To memorize the serum dosages in botulism: A and E are 10 thousand each (AE-10), and B is half that amount (5 thousand).
Class and exam questions
Which forms of existence Entamoeba histolytica are pathogenic?
The tissue and large vegetative forms (trophozoites) are pathogenic.
What is the main transmission mechanism of amebiasis?
The main transmission mechanism is fecal-oral, most commonly realized via the foodborne route.
What else to study on this topic
- Morphological differences between pathogenic and non-pathogenic amebae
- Virulence factors of Entamoeba histolytica
- Pathogenesis of extraintestinal amebic abscess formation
- Features of bulbar syndrome in various infections
- Bioassays in the diagnosis of neuroinfections
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