• acute viral infectious disease of CNS, with myeloencephalitis, leading to death.
• Viral factors: RNA virus – Rhabdoviridae family

• Rabies virus - can be rapidly inactivated by exposure to ultraviolet light, sunlight, desiccation, formalin, phenol, ether, detergents.
• The virus is unstable at extreme ranges of pH. Virion infectivity remains stable for long periods of time if the virus is properly frozen or evenmaintained at approximately 4C.

• Rabies is primarily a disease of animals
• Reservoir – wild animals: fox, wolf, raccoon dog, bat, badger.
  squirrels, mice, rats
• Source of infection - dogs, cats, bats.
• occasionally- other animals- cows, deer, rodents, -non important – in epidemiologic chain

• Most cases of human rabies occur following animal bites – virus transmitted by infected saliva – bite transmission
• Rarely non-bite transmission:
  by aerosols, by person-to-person transmission (corneal transplants),
  contact of the broken skin, mucous membranes, conjunctiva with infected saliva or the brain (veterinarian, laboratory staff)

• Rabies is highly neurotropic, restricted to nervous tissue throughout most of the course of infection in animal and human.
• Initial phase of local replication of rabies virus at the inoculation site prior to transmission into the CNS (rapid virus replication in grey matter)
• An extremely important component of disease is the centrifugal spread of virus back out of the CNS to peripheral sites ( salivary and submaxillary glands, lungs, kidney, skin)

• Incubation period - is usually between 20 and 90 days.
  95% of the cases have incubation periods less than 1 year, although several well-documented cases have occurred 1-6 years or more after exposure.
• Most dangerous: extensive exposure (broad bites) near CNS (face) or places well supplied with blood (neck or reproductive organs)

• Prodromal symptoms: are often non specific:
  malaise, fatigue, headache, anorexia, fever,
  cough, chills, sore throat, abdominal pain, nausea, vomiting, diarrhea.
• In 50% of the patients, pain or paresthesia referred to the site of the exposure is the first rabies - specific symptoms.

• Period of acute neurologic symptoms:
  Furious rabies: hyperactivity, disorientation, hallucinations, bizarre behavior, hydrophobia (severe spasm of the pharynx, larynx and diaphragm – released by the sound or sight of running water), opisthotonus
  Paralytic rabies - about 20% of the patients

• The acute neurological phase lasts 2-7 days, with longer durations in the paralytic forms. It ends either with an abrupt death or progression to a coma and after short time - the patient dies.

• History – animals bites
• Characteristic clinical manifestations (rabies has the highest case fatality rate of any known human infections – essentially 100% )
• In living patients – serological tests - immunofluorescent rabies antibody staining of skin biopsies, in CSF, in urine.
  PCR- good method for saliva samples.

Negri bodies – characteristic cytoplasmic inclusions
Present in 70-80% of cases.
They are particularly common in the hippocampus, in the horn of Ammon, in the Purkinje cells of the cerebellum.

The principles used to control rabies in domestic animals - restriction of movement, stray animal control ordinances and mandatory vaccinations.
Mass-vaccination of wild forest animals.

• Prophylactic vaccinations:
  veterinarians, laboratory staff, foresters
• Post-exposure prophylaxis 2018q:
  after bites of wild animal - each case
  after bites of unknown domestic animal - each case
  after contact of the broken skin, mucous membranes, conjunctiva with infected saliva or brain tissue- each case

Local - wound disinfection and surgical treatment
Active - immunization (vaccine)
Both active and passive immunization: vaccine (no time limit) + immunoglobulines (up to 7 days after 1 dosis vacci)

• Particularly dangerous form of poisoning, most frequently by the alimentary way, caused by damage of a part of cholinergic nervous system by the botulism

• Clostridium botulinum
  gram-positive, heat-resistant anaerobic, sporeforming bacilli
  produce neurotoxin
  The most effective biological toxin
  There are 7 types of C.botulinum (A-G)

Consumption of the product contaminated with Clostridium botulinum rod, with produced already toxin,
A, B and C toxin types: separate poisonings of humans with type F and G (this type causes a sudden death without any paralytic symptoms),
Type A (occurs more seldom),
Type B (most frequent occurrence in Poland),
Mainly in the preserved products 
(particularly home-made preservatives: pates, vegetables),
Type E - after consumption of fish preservatives 
(Japan, Alaska, Scandinavian countries)

Incubation period: 2- 4 days
(The shorter incubation period the worse prognosis – regards the time from the consumption of the food to the moment of the first neurological symptoms occurrence)

• The triad of symptoms – very characteristic, occurs in every case:
  sight disorders: double vision, eyelid fall, blurred vision, pupils are widened, with complete lack of reaction to light or delayed, slow reaction
  dryness in the mouth cavity and swallowing disorders: inhibition of secretion of saliva, paralysis of cholinergic system
  constipation and urine retention: smooth muscles paralysis

• Differentiatial diagnosis:
  With atropine or phosphor-organic compounds poisoning
  With bulbar paralysis in the course of cerebritis,
  With methyl alcohol intoxication

• Revealing the presence of the toxin in the blood (tests on laboratory animals – confirmation of diagnosis and at the same time indication of the toxin type),
• The blood for tests should be taken before serum administration to patients – antitoxins,
• Confirmation of the presence of the rods or their toxins in the consumed food or vomit, when the result is positive – confirms the diagnosis

Immunoglobulines – 
(human or obtained from animals) – polyvalent: A, B /E
Antibiotics 
(in more severe cases - prevention from complications like bacterial or aspiration pneumonia),
Vitamins, Nutrition, Respiration support, Rehabilitation

Serious/bad – in severe cases (death due to general paralysis or complications e.g. respiratory insufficiency, aspiration pneumonia),
Good – in mild cases (gradual recovery: relatively long-term maintained symptoms of nervous –muscular synapses inhibition)