Inflammation of the lining of the spinal cord in dogs. Symptoms and treatment of meningitis in dogs. Vaccination as a reliable method of prevention



Meningitis is a generalized name for diseases in which the leading symptom is inflammation of the membranes of the brain and spinal cord, characterized by a deep disorder in the functions of the cortex, subcortical and autonomic centers.

Distinguish:

1. Pachymeningitis - inflammation of the dura mater.

2. Arachnoiditis - inflammation of the arachnoid mater.

3. Leptomeningitis - inflammation of the pia mater and arachnoid.

Meningitis is accompanied by increased intracranial pressure and cell-protein dissociation (high pleocytosis with normal or slightly elevated protein numbers). In the clinic, the term "meningitis" most often refers to leptomeningitis.

According to the predominant localization, meningitis is divided into cerebral (covexital and basal) and spinal forms.

Meningitis is divided depending on the type of pathogen into:

Bacterial (purulent, non-purulent),

Viral,

Rarely - fungi, mycoplasmas, rickettsia, amoeba, helminths.

According to the nature of exudation, meningitis is divided into:

Serous (viral, tuberculosis, syphilitic),

Purulent (usually any bacterial).

By origin: primary or secondary.

Pathogen.

Meningococci are pairwise arranged gram-negative spherical formations; in the cerebrospinal fluid, they are localized intracellularly and have the shape of a coffee bean. In external environment quickly die. There are various serotypes of the pathogen (A, B, C, etc.). Sensitive to penicillin, chloramphenicol, tetracyclines. Gate of infection - mucous membrane of the upper respiratory tract. In most cases, the presence of meningococci on the mucous membrane does not lead to the development of the disease (carriage).

Etiology.

The main reason is infection. The most important are: viral meningoencephalitis caused by neurotropic or pantropic viruses - rabies, Aujeszky's disease, equine infectious encephalitis, malignant catarrhal fever, canine distemper, etc.

With thiamine deficiency, cerebrocortical necrosis (polyencephalomalacia) develops in calves, high level ammonium leads to uremic encephalopathy. Sometimes it can occur on an allergic basis or intoxication. Hypothermia, overheating and other factors that reduce the body's resistance also contribute to the onset of the disease.

Pathogenesis.

With meningitis of an infectious nature, the pathogen enters the meninges and brain by the hematogenous or lymphogenous route. Neurotropic viruses with affinity for nervous tissue penetrate the CNS along nerve fibers. Inflammatory process in the meninges, subarachnoid space, gray and white matter is accompanied by inflammatory-destructive processes in nerve cells. The main form of tissue reaction in meningitis in acute period is arterial hyperemia with vascular infiltration, hemorrhages, proliferation of microglia and nerve fibers (demyelinization). There is diffuse infiltration of the nervous tissue. As a result of irritation of the receptors of the meninges, edema (hydrocephalus) develops, due to increased secretion of cerebrospinal fluid by the choroid plexuses, which has become an obstacle to liquor circulation. Depending on the localization of the inflammatory process, various focal symptoms also occur.

Symptoms.

At the beginning of the prodromal period, body temperature rises, shortness of breath appears, and appetite decreases. Depending on the localization of the process, a combination of cerebral and focal symptoms develops. Cerebral symptoms are characterized by depression, lethargy, impaired coordination of movements. The gait becomes shaky, the animal raises its legs high, stumbles. Reflexes are reduced or disappear. A few hours after infection, with a predominant lesion of the meninges, a fit of excitement, anxiety, trembling, and photophobia occurs. Meningeal syndrome develops, which is characterized by dilated pupils, immobility of the eyeballs, hypersensitivity to noise and light, stiffness of the muscles of the neck and neck, hyperesthesia of the skin, increased tendon reflexes, paresis and paralysis of the limbs, as well as tremor and paralysis of the limbs. In the future, progressive depression, vomiting in dogs and pigs, a disorder in the act of swallowing, disorders of the autonomic regulation of the cardiovascular, respiratory and digestive systems are observed.

With damage to the cerebral cortex and its membranes, focal symptoms of CNS damage develop. The characteristic clinical signs of the syndrome of brain damage are strong excitement, aggression, drowsiness, convulsive muscle contractions, weakening of conditioned reflexes. With the loss of the function of the cerebral cortex, all reactions to auditory, visual and olfactory stimuli disappear. With the defeat of the oblongata, death can occur from paralysis of the respiratory and vasomotor centers.

Focal symptoms are manifested by trembling of the eyeball, uneven pupil dilation, strabismus, lowering of the upper eyelid, lowering of the ear, drooping of the lower jaw.

Pathological changes:

Hyperemia of the membranes and vessels of the brain, edema and infiltration of its individual sections are noted. In the subarachnoid space cloudy yellow or reddish fluid or purulent exudate.

Treatment of meningitis includes etiotropic, pathogenetic, symptomatic and restorative therapies.

Etiotropic therapy: with the viral nature of the disease, sera, gamma globulins, immunoglobulins are used as specific agents for various kinds animals. Antivirals are also used non-specific means therapy: leukocyte interferon, reaferon, betaferon. In secondary meningitis, antibiotics are used (penicillin, ampicillin, ampioks, cefazolin, klaforan) and sulfonamides in maximum dosages. Preferred drugs are penicillin antibiotics and cephalosporins.

Interferons: a group of endogenous low molecular weight proteins with antiviral, immunomodulatory effects. Cells affected by the virus begin to produce and secrete into environment a special protein that prevents the reproduction of the virus in cells.

Interferon is obtained from a nutrient fluid in which human leukocytes or fibroblasts are cultured. In response to exposure to the interferonogen virus. Interferon itself does not have an antiviral effect. It interacts with special binding sites on the cell surface, which leads to the activation of protein kinase and the formation of a low molecular weight inhibitor of protein synthesis that stimulates endonucleases that destroy the RNA of viruses and host cells. Apart from antiviral action it is able to activate reduced immunity by increasing the phagocytic activity of macrophages and killer cells, and also affect the functions of the central nervous system.

Side effects when topical application no. With parenteral administration, fever, lowering blood pressure, tachycardia, impaired hematopoiesis and central nervous system functions (loss of appetite, vomiting) may occur. The drug is excreted by the kidneys, so if they are damaged, it cannot be prescribed.

Leukocyte interferon (Interferonum leucocyticum humanum siccum): obtained from human donated blood. Porous powder of grayish-pink color, soluble in water. Used in the form of a solution, which is prepared in distilled or boiled water. Apply the inhalation method of administration.

Reaferon (Reaferonum): recombinant alpha2-interferon produced by a bacterial strain of Pseudomonas, in the genetic apparatus of which the human leukocyte interferon gene is inserted. porous powder, white color, soluble in water. Assign in / m or s / c. for IM and s / c administration, the contents of the vial are dissolved in 1 ml of water immediately before administration. When applied, chills, allergic manifestations are possible. Contraindications: allergic diseases, kidney and liver diseases, pregnancy. Release form: 3; 5 million IU in vials.

Antibiotics: antibiotics of the penicillin and cephalosporin series are bactericidal drugs that cause the death of microorganisms. They give a quick therapeutic effect in severe infectious diseases. They are able to inhibit the biochemical processes occurring in microorganisms. According to the mechanism of action, they are classified as inhibitors of the microbial wall or its components. Penicillins also have the property of inhibiting the adhesion of microorganisms to cell membranes. They are also antibiotics. a wide range actions affecting gram-positive and gram-negative cocci, and some rods. Microbial resistance to these groups is also low.

Penicillins: by chemical structure they are derivatives of 6-aminopinicillanic acid containing various substituents on the amino group. Mechanism antimicrobial action is to disrupt the formation of the cell wall from pre-synthesized murein. Toxicity is low. The main side effects are allergic reactions, they are associated with the formation of antibodies. And also an annoying effect.

Ampiox (Ampioxum): a combination drug containing ampicillin and oxacillin. The drug acts on gram + (staphylococcus, streptococcus, pneumococcus) and gram- (gonococcus, meningococcus, E. coli, salmonella). Due to the content of oxacillin, it is active against penillinase-forming staphylococci. The drug penetrates well into the blood when parenteral and ingestion. Side effects: pain at the injection site, when taken orally - nausea, vomiting, allergic reactions.

Ampicillin (Ampicillinum): white crystalline powder, bitter taste. Semi-synthetic antibiotic, by acylation of 6-APA with an aminophenylacetic acid residue. It has a wide spectrum of action, but it does not act on penicillin-forming staphylococci, as it is destroyed by penicillinase. With prolonged use, there is a possibility for the development of superinfection.

Cephalosporins: Like penicillins, they are beta-lactam antibiotics. They act bactericidal. Broad-spectrum, resistant to penicillinase, but some are destroyed by cephalosporinases. Produced by gram - microbes (Pseudomonas aeruginosa, Enterobacter)

Cefazolin (Kefzol) (Cephazolini): Available as sodium salt-white lyophinized mass, soluble in water. Cefazolin is not absorbed when taken orally; when administered intramuscularly, the drug is rapidly absorbed. It is excreted by the kidneys unchanged. Cefazolin crosses the placental barrier and is found in amniotic fluid. Enter vm, vv drip. When administered intramuscularly, local soreness and allergic reactions are possible.

Klaforan (cefotaxime) (Cefotaxim): third generation. Apply vm and vv. when administered intramuscularly, it is rapidly absorbed. The bactericidal concentration remains in the blood for 12 hours. It penetrates well into tissues and body fluids (pleural, peritoneal, synovial). Excreted in urine and bile.

pathogenic therapy. Aimed at:

1. dehydration and fight against cerebral edema. (10-20% solution of mannitol, 1-1.5 gkg IV, furosemide, dicarb).

2. removal of inflammation (prednisolone 0.5 mgkg, dexamethasone 0.15 mgkg each).

3. improvement of brain microcirculation (nootropil, cavinton, trental, cerebrolysin, actovegin).

4. detoxification (polyglucin, reopoliglyukin, hemodez, reogluman).

5. maintenance of homeostasis and water and electrolyte balance (5% glucose solution, potassium chloride, 4% sodium bicarbonate solution, isotonic solution sodium chloride).

6. elimination of cardiovascular disorders (20% camphor solution, sulfocamphocaine, cardiac glycosides)

7. restoration of brain metabolism (vitamins of group B and vitamin C, PP).

8. prevention of superinfection when using antibiotics (nystatin, levorin).

1. Mannitol (Mannitolum): the active substance is the hexahydric alcohol mannitol, to which antiseptic agents (sulfacyl sodium, tripaflavin) and sodium chloride are added. It has a strong diuretic effect, accompanied by the release of water and sodium salts from the body. Indications for use - cerebral edema. Vv on 5% glucose or isotonic sodium chloride solution.

Furosemide (Furosemidum): a fast-acting diuretic (saluretic) is a diuretic that enhances the release of sodium and chlorine. The diuretic effect is associated with inhibition of the readsorption of sodium and chloride ions in the proximal and distal parts of the convoluted tubules and in the ascending parts of the loop of Henle. Contraindicated in hypokalemia, renal failure and obstruction.

Diacarb (Diacarb): A diuretic that inhibits the activity of carbonic anhydrase. Inhibition of carbonic anhydrase leads to a decrease in the formation of carbonic acid and a decrease in the readsorption of bicarbonate and sodium by the epithelium of the renal tubules, the excretion of sodium and bicarbonate and water in the urine increases, the pH of the urine rises.

2. Prednisolone (Prednisolonum): glucocorticosteroid (adrenal hormone). It has an anti-inflammatory and desensitizing effect, has an antiseptic and anti-shock effect, reduces capillary permeability.

Dexamethasone (Dexamethasonum): a glucocorticosteroid hormone with strong anti-allergic and anti-inflammatory properties.

3. Nootropics do not have a pronounced psychostimulating or sedative effect, do not cause specific changes bioelectric activity brain. They stimulate the transmission of excitation in the central neurons, facilitate the blood supply to the brain, and increase its resistance to hypoxia. They affect metabolic processes in the nerve cell: activation of protein and RNA synthesis, improved glucose utilization, increased ATP synthesis.

Piracetam (Piracetam) stimulates redox processes, improves regional blood flow and ischemic areas. Improvement of energy processes under the influence of priracetam leads to an increase in the resistance of brain tissues during hypoxia and toxic effects.

Sodium oxybutyrate (Natrii oxybutyras): the sodium salt of gamma-hydroxybutyric acid. In addition to the antihyppoxic action, it has a sedative and central muscle relaxant effect. It does not have an analgesic effect, but enhances the effect of analgesics, and is characterized by an anti-shock effect. With prolonged use, hypokalemia may develop.

4. Plasma-substituting drugs are divided into a number of groups - large and low molecular weight. Large molecular compounds (polyglucin, reopoliglyukin, gelatinol) have hemodynamic and detoxifying properties. Low molecular weight (hemodez and polydez) are used for detoxification and, to a lesser extent. For hemodynamic purposes. Hemodynamic preparations have a large molecular weight close to that of blood albumin. They do not penetrate vascular wall tissues are not filtered in the glomeruli of the kidneys and therefore circulate in the blood stream for a long time. These macromolecular compounds maintain the oncotic pressure of the blood plasma and contribute to the preservation of BCC, and thereby increase blood pressure.

Polyglucin (Polyglucinum): 6% solution of dextran (glucose polymer). The drug is non-toxic and is excreted by the kidneys on the first day. A small amount of it is gradually broken down to glucose. But the drug is not the source carbohydrate nutrition. used for prophylactic and therapeutic purposes with traumatic, surgical and burn shocks, with acute blood loss, with intoxication.

Reopoliglyukin (Rheopolyglucinum): 10% dextran solution in isotonic sodium chloride solution. Low molecular weight. It promotes the movement of fluid from tissues into the bloodstream, resulting in a decrease in blood viscosity, restoration of current in small capillaries, a decrease in aggregation of formed elements, and a detoxification property.

Hemodesum (Haemodesum): an aqueous saline solution containing 6% low molecular weight polyvinylpyrrolidone. Used for intoxication. The mechanism of action is associated with the ability of low molecular weight polyvinylpyrrolidone to bind toxins circulating in the blood and quickly remove them from the body. The drug is excreted by the kidneys and partially through the intestines. It increases blood flow in the kidneys, increases glomerular filtration, increases diuresis. Reduces pressure somewhat.

5. The sodium ion is found mainly in blood plasma and extracellular fluid, maintaining osmotic pressure and polarization of cell membranes in them. Its penetration through the membrane causes the emergence of both an excitatory postsynaptic potential and an action potential, without which neither the transmission of nerve impulses nor the function of almost all organs and tissues of the body is possible. Sodium chloride isotonic solution (Solutio Natrii chloridi isotonika) is mainly used as a sodium preparation. pro injectionibus): used to compensate for the loss of water and sodium in various forms of dehydration. For this purpose, it is infused together with a 5% Glucose Solution (Solucio Glucosum 5%): which is considered as a source of water, since glucose quickly burns out.

Potassium ions are contained mainly inside the cells, maintaining the polarization of cell membranes, stimulating the activity of many enzyme systems. Potassium chloride (Kalii chloridum): a 4% solution of the drug in a 40% glucose solution is used intravenously. Also potassium preparations are: panangin, asparkam.

6. Under the analeptic drugs mean a group medicinal substances excitatory vasomotor and respiratory centers medulla oblongata.

Camphor (Camphora): with the introduction of a PC solution of camphor in oil, they tone up the respiratory center, stimulate the vasomotor. Camphor has a direct effect on the heart muscle, strengthening it metabolic processes and increasing its sensitivity to the influence of sympathetic nerves. Under its influence, peripheral vessels narrow. Apply a solution of camphor in oil 20% for injection (Solucio Camphorae oleosae 20% pro injrctionibus).

Sulfocamphocaine 10% for injection (Sulphocamphocainum 10% pro injectionibus): a complex compound of sulfocamphoric acid and novocaine base. It is similar in action to camphor, but due to solubility in water, it is quickly absorbed with SC and IM administration, does not lead to the formation of infiltrates.

7. Thiamine (Tiaminum): thiamine bromide and thiamine chloride are used. The main indications for use are hypo- and avitaminosis B1, as well as neuritis, neuralgia radiculitis, peripheral paralysis.

Pyridoxine (Pyridoxinum): Necessary for the normal functioning of the CNS and PNS.

Ascorbic acid (Acidum ascorbinicum): it has strong reducing properties. It takes part in the synthesis of procollagen and collagen and the normalization of capillary permeability, in redox processes, carbohydrate metabolism, blood clotting, and the formation of steroid hormones. Not synthesized in the body.

Nicotinic acid (Acidum nicotinum): it is used for spasms of the vessels of the extremities, the brain, and infectious diseases. It is a prosthetic group of enzymes.

8. Nystatin (Nystatinum): an antibiotic of the polyene group. It acts on pathogenic fungi and especially on yeast-like fungi of the genus Candida, as well as aspergella. Applied for prophylactic purposes with prolonged use of antibiotics penicillin and other groups.

Levorin (Levorinum): has chemotherapeutic activity against pathogenic yeast-like fungi, in particular fungi of the genus Candida. In some cases, it works when nystatin is ineffective.

Symptomatic therapy: aimed at stopping the anxiety of the animal and status epilepticus. For this purpose, apply:

1. Sedatives (phenobarbilal 4-6 mg/kg daily, deazepam 0.25-0.5 mg/kg, chloral hydrate)

2. With paresis, hyperkinesis, epileptic seizures, drugs are prescribed that improve brain metabolism and muscle tissue(ATP, cocarboxylase, cerebrolysin).

Phenobarbital (Phenobarbitalum): a derivative of barbituric acid. The mechanism of action is associated with a decrease in the excitability of neurons of the epileptic focus, under the influence of the drug. It has a hypnotic effect, has a calming effect in small doses.

Chloral hydrate (Chlorali hydras): sedative, hypnotic and analgesic. It has a complex effect on the central nervous system; in small doses it causes a weakening of inhibitory processes, in large doses it causes a decrease in excitation processes.





Inflammatory diseases nervous system in dogs are dangerous with serious consequences. With big share probability they can end in death, and if not, then the consequences in the form neurological pathologies often make the dog disabled for life. If the dog has impaired coordination of movements, there is a loss of muscle tone, stiffness cervical, overreaction to ordinary stimuli, it can be assumed that she has meningitis.

Meningitis in dogs is an inflammation of the lining of the brain and spinal cord. The difficulty of recognizing an ailment is that it can have many causes and the most different etiology. And, nevertheless, it is very important to conduct a competent diagnosis and start treatment on time. Then the chances of recovery of the animal will increase significantly. How dangerous is meningitis, is it treatable, is there a meningitis vaccine? About this in our article.

Head and spinal cord dogs have hard, soft, and arachnoid coats, all of which are prone to inflammation. If the dura mater is affected, then the disease is called pachymeningitis, pathology of the soft and arachnoid inflammatory nature called leptomeningitis or simply meningitis. If only the arachnoid membrane is inflamed, then arachnoiditis is diagnosed.

The disease is most often secondary character, that is, is dangerous symptom others infectious diseases. But, in more rare cases, when pathogens hit directly on the meninges, it is a disease of the primary type. Secondary meningitis in a pet is not dangerous to humans, but in the case of primary inflammation, microbes or viruses that have affected the brain can be contained in all biological fluids and mucous membranes, including oral cavity. Therefore, for owners and other people in contact with a sick dog, it is important not to forget about certain safety measures.

Types of disease and ways of infection

Meningitis in dogs is classified according to several criteria.

By type of pathogen (etiology), there are several varieties of infectious forms of the disease. Most often they are purulent lesions of the brain. In this case, in cerebrospinal fluid(liquor) neutrophils (leukocyte cells) predominate:

  • bacterial meningitis (causative agents - pneumococci, meningococci, mycobacterium tuberculosis);
  • viral (enteroviruses);
  • fungal (candida, cryptococci);
  • protozoan (a consequence of toxoplasmosis).

In addition, there are aseptic forms of the disease, representing, most often, serous (non-purulent) forms (in this case, lymphocytes will prevail in the cerebrospinal fluid):

  • meningitis caused by helminths;
  • various toxins (chemical and organic);
  • autoimmune reactions.

With the disease, there are several ways of infection of the meninges:

  • contact path (consequence of purulent infection);
  • sinusogenic (complication of nasal infection - sinusitis, sinusitis);
  • otogenic (complication of ear infections);
  • ondogenic (complication of dental infections);
  • infections can affect the brain by lymphogenous, hematogenous, placental routes;
  • meningitis may develop traumatic injury cranium.

Forms of the disease differ in the nature of the lesion and involvement:

  • generalized (cerebral) meningitis;
  • limited (focal form).

Causes and provoking factors

Most often, meningitis in dogs becomes a complication of various serious diseases:

Young dogs and old people are most susceptible to the disease. The immune system puppies and older dogs is the weakest, which makes a high probability of complications of a wide variety of and, at first glance, benign infections.

Symptoms of the disease

Meningitis can have very extensive symptoms in dogs. Their list includes several groups.

Symptoms inherent in any infection

First of all, pay attention to the presence of the so-called general infectious symptoms in the dog:

  • high body temperature, fever, dry and hot nose;
  • rapid breathing, shortness of breath;
  • violation of the heart rate (tachycardia or bradycardia);
  • intoxication;
  • lack of appetite, vomiting.

meningeal syndrome

Meningeal syndrome includes cerebral symptoms:

  • pathological tension of the muscles of the neck and upper back;
  • stiffness of the neck muscles, the dog cannot unbend;
  • incoordination, unsteady gait;
  • when involving cranial nerves inhibition of reflexes is observed;
  • headaches of a bursting nature, localized in the back of the head and radiating to the neck;
  • gag reflex that occurs when trying to change the position of the body;
  • hypersensitivity (rigidity) to stimuli. Painful reaction to light, noise, smell.

Focal symptoms

Focal symptoms occur when various parts of the brain structures are involved in the process:

  • paralysis of the limbs;
  • pupil dilation;
  • disorder of the act of swallowing;
  • trembling of the eyeballs;
  • lowering of the upper eyelid;

If the medulla oblongata is damaged, the respiratory center may be damaged, which will inevitably lead to death.

Diagnostic methods

If meningitis is suspected, the animal should be referred to a well-equipped hospital as soon as possible. veterinary clinic for diagnosis and treatment. After an external examination, the doctor must take diagnostic measures.

The most informative way to diagnose meningitis is to take cerebrospinal fluid (CSF) for examination by lumbar puncture. The procedure is carried out under general anesthesia. After taking a fluid sample, describe the state of the CSF, general form, protein content, conduct a cytological study. The following data indicate the presence of the disease:

  • when taking a puncture, the cerebrospinal fluid flows out under great pressure;
  • at serous meningitis- presence of lymphocytes, transparent consistency;
  • at purulent meningitis- the presence of neutrophils, cloudy consistency, brown color, reduced to zero glucose content;
  • with tuberculous or fungal meningitis - reduced glucose levels.

In addition, to clarify the diagnosis, the following diagnostic methods are prescribed:

  • craniography (radiography of the skull without the use of contrast agents);
  • magnetic resonance imaging or computer diagnostics;
  • electroencephalography;
  • clinical analysis of blood and urine.

Must be carried out differential diagnosis to rule out diseases

  • hydrocephalus;
  • renal failure;
  • rabies;
  • leptospirosis;
  • distemper.

Treatment of the disease

After clarifying the diagnosis and identifying the etiology of the disease, the doctor, in accordance with the developed scheme, begins drug treatment. Only those drugs that tend to penetrate the blood-brain barrier are prescribed.

  1. The bacterial nature of meningitis is treated with antibiotics of the penicillin and cephalosporin series (Ampicillin, Cefazolin) and sulfonamides (Enroxil).
  2. Viral meningitis is treated antiviral agents based on gamma globulin and enterferon. In addition, appoint symptomatic treatment, facilitating general state: decongestants (Furasemide), antispasmodics (No-Shpa), painkillers (Ketanov).
  3. For the treatment of tuberculous meningitis, complex antibiotic therapy is used. Specially designed combinations of antibiotics are used: (Isoniazid and Streptomycin). With the development of complications, anti-tuberculosis drugs (Rifampicin) are used.
  4. If meningitis appears neurological symptoms, then nootropics and sedative drugs (Cerebrolysin, Diazepam) are used.
  5. Aseptic forms of the disease are treated with non-steroidal anti-inflammatory drugs and corticosteroids (Ibufen).
  6. Supportive therapy consists in the appointment of vitamins of groups C and B.

Forecast and prevention

The percentage of the probability of a successful outcome of the disease for a dog depends on the stage at which it was detected, how dangerous its form is. The timeliness and adequacy of therapeutic measures are very important.

Most animals after recovery acquire serious neurological consequences, which require long-term rehabilitation or lifelong treatment to eliminate:

  • headaches;
  • bouts of aggression;
  • increased intracranial pressure;
  • epileptic syndrome;
  • significant impairment of vision and hearing.

There is no vaccine for meningitis because the etiology of the disease is very diverse. But it is possible to protect an animal from most infections complicated by inflammation of the meninges by timely vaccination with complex polyvalent vaccines.

In addition, it is necessary throughout life to protect the pet in every possible way from possible colds and viral diseases, carry out sanitation of foci of infection. Dogs should not be allowed to come into contact with sick animals.

It is recommended to constantly monitor the mood of the pet, his appetite, physical activity. In case of any changes, features of behavior, without delay, you need to take him to the veterinarian. Only the attentiveness of the owner to his pet will help save his life, since the disease can be cured only by early stage until the virus hit deep structures brain.

Author: Georgina Child, BVSc, DACVIM (Neurology) / Specialized Clinic for small animals, 1 Richardson Pl, North Ryde NSW 2113

Inflammatory diseases of the CNS affect the brain, meninges and/or spinal cord. Majority pathological processes that cause meningitis also lead to concomitant encephalitis and/or myelitis. In dogs, non-infectious and (presumably) immune-mediated forms of meningoencephalomyelitis are much more common than infectious forms.

The causes of most immune-mediated disorders have not been established.

Immune-mediated diseases are believed to include corticosteroid-responsive meningoencephalitis, granulomatous meningoencephalomyelitis (GME), necrotizing vasculitis, necrotizing meningoencephalitis (NME) in certain breeds (Pug, Maltese, Chihuahua), and necrotizing leukoencephalitis (in yorkshire terriers).

The final diagnosis is based on the results histological examination; in most cases, it is not possible to make an intravital diagnosis without histological examination, since clinical signs and results laboratory research are often nonspecific and indistinguishable from those of infectious meningoencephalomyelitis, vascular diseases and some CNS tumors. Differences in the histological pattern in non-inflammatory meningoencephalitis may or may not reflect different reasons or immunological mechanisms.

Corticosteroid-responsive meningitis (polyarteritis, necrotizing vasculitis, beagle pain syndrome)

Steroid-responsive meningitis occurs predominantly in young dogs. large breeds (average age 1 year), although it happens with more small breeds(for example, polyarteritis in beagles (also called pain syndrome Beagles), Nova Scotia Retrievers and Italian Greyhounds, noted in recent times).

Symptoms characteristic of meningitis include back pain, unnatural posture, stiff gait, lethargy, and lethargy. Fever is common, with clinical analysis blood may show leukocytosis. Clinical signs are both acute and severe, and episodic. Neurological disorders (paresis / paralysis) are rare, but possible with damage to the spinal cord or, in rare cases, the brain. Cases of necrotizing vasculitis of soft and arachnoid shells spinal cord in young Beagles, German Shorthair Pointers and Bernese mountain dogs sometimes found in other breeds.

Clinical signs are similar to those seen in steroid-responsive meningitis, but symptoms of multiple or focal spinal cord involvement may be present.

Treatment is similar to that used for meningitis, but the prognosis depends on the degree of spinal cord involvement.

CSF usually shows marked pleocytosis with neutrophils up to >10,000/mcL. Between episodes, CSF results may be normal. Microorganisms in the CSF are absent, culture results are negative. Some animals develop concomitant polyarthritis. Treatment consists of a long-term course of corticosteroids at an initial dose of 2–4 mg/kg per day, which is gradually reduced over 3–6 months.

Animals with only symptoms of meningitis have a good prognosis, although relapses are common. If corticosteroids are ineffective or the animal does not tolerate side effects you can use azathioprine.

Steroid-responsive meningitis occasionally occurs in cats.

For a more accurate designation of the diagnosis, the term "meningoencephalitis (or meningoencephalomyelitis) of unknown etiology (or origin)" (MNE or MNP) has been proposed. Other proposed or previous terms include nonpathogenic meningoencephalomyelitis, noninfectious inflammatory disease of the CNS, nonsuppurative meningoencephalitis, reticulosis, and others.

In this paper, the term GME will be used to describe all non-infectious inflammatory diseases of the CNS (even if it is incorrect), since it is generally accepted. These diseases are widespread throughout the world and can account for up to 25% of all cases of CNS disease in dogs.

GME is most widely distributed in dwarf and small breeds, especially maltese lapdogs, pygmy poodles and all terriers (including Staffordshire and Airedale). However, it can develop in any breed of dog, including large dogs and mestizos. The disease is most common in middle-aged dogs (rarely in dogs<2 лет или >10 years). The disease occurs in both sexes, but it is possible that females get sick more often.

Diagnosis of non-infectious inflammatory disease CNS is placed on the basis of clinical signs and exclusion infectious causes- often based on results serological study, CSF analysis and brain imaging using imaging methods. However, in many cases, a presumptive diagnosis is made based on the best guess based on breed, age, history, and clinical signs. An inflammatory disease of the CNS is characterized by acute development of symptoms of multiple CNS lesions (brain or spinal cord) and / or hyperesthesia (in the cervical or lumbar-thoracic region). Clinical features include symptoms of the lesion forebrain(change of mental state, obsessive movement in a circle, convulsions) and / or caudal fossa (ataxia, vestibular disorders, disorders of the cranial nerves) and / or lesions of the spinal cord (at any level). In many cases, it is difficult to determine the anatomical localization of the lesion. However, the disease is chronic, progressive, and in some cases appears episodic, with a significant number of dogs presenting with focal neurological symptoms. Animals with meningitis often suffer from severe pain in the neck, take a hunched posture, there is a reluctance to move and a constrained "stilted" gait. many owners small dogs note that the animal is hiding, whining or screaming without apparent reason when trying to pick it up. Often there are back pains of uncertain localization. However, signs of back pain are not observed in all cases.

There may be symptoms of focal lesions of the spinal cord (any department, but most often the cervical), including paresis or paralysis. A form of GME accompanied by neuritis has been described optic nerve however, it is rare. Clinical signs may be acute and rapidly progressive, or insidious and slowly progressive over weeks or months.

In general, GME can have any history, be accompanied by any neurological symptoms, and develop in dogs of any age and breed!

Attempts have been made to classify forms of GME as disseminated, focal, or proceeding with damage to the optic nerve. This is very difficult to do in vivo and does not always matter for diagnosis, treatment and prognosis. Breed necrotizing meningoencephalitis (in Pugs, Maltese, Chihuahuas and Yorkshire Terriers) can develop in young age (<1 года, особенно у мальтийских болонок и мопсов), но встречается и у собак старше (особенно у чихуахуа). Обычно такой энцефалит развивается остро с симптомами тяжелого поражения переднего мозга, включая судороги. Неврологические нарушения часто быстро прогрессируют. Эти заболевания у разных пород классифицируются в зависимости от поражения оболочек, преимущественного поражения белого вещества и локализации (большие полушария или ствол мозга, или обе части). Такие различия могут отражать разные патологические процессы либо различия иммунного ответа, возможно, генетические.

Usually, clinical examination, clinical and biochemical blood tests of dogs with any form of non-infectious inflammatory diseases of the central nervous system do not show abnormalities. Fever is possible, but rare.

CSF analysis usually shows mild to moderate pleocytosis with a predominance of mononuclear cells and varying degrees of protein elevation. The total concentration of leukocytes varies from<10 до >5000 cells. The protein concentration can be from normal to 4 g/l. Neutrophils usually make up less than 50% of all detected cells. Sometimes there are macrophages and single eosinophils. In some dogs (sometimes more than 10%), CSF analysis shows no abnormalities. Changes in the composition of the CSF may indicate inflammation, which is the basis for suspicion of GME, but a similar pattern of CSF is possible in other diseases, including infectious, vascular (heart attack), and neoplasms. In most cases, CSF analysis is not sufficient to make a definitive diagnosis, but it can provide clarifying information when looking for a likely diagnosis in cases of spinal cord or brain damage. CSF analysis detects inflammation, but only if the inflammation involves the meninges, the ependymal lining, or tissues close to the CSF pathways. Nonspecific changes in the CSF are often observed in vascular, traumatic, degenerative, neoplastic and inflammatory diseases of the central nervous system.

In animals with elevated intracranial pressure (ICP), CSF sampling is associated with significant risk and may result in brain herniation at the incision of the cerebellar tentorium or herniation of the cerebellum at the foramen magnum. CSF sampling is also risky in severe brain disease, including without increased intracranial pressure, when changes in brain perfusion and reduced brain capacity for self-regulation can lead to further deterioration of neurological status.

Unfortunately, it is in these animals that CSF analysis often provides the most valuable diagnostic information. Clinical signs of elevated ICP include dizziness, stupor, dyspnea, head-butting, bradycardia, and elevated blood pressure. Some animals with elevated intracranial pressure have no obvious clinical signs.

CSF withdrawal from the cisterna also carries the risk of damage to structures of the nervous system (spinal cord or medulla oblongata), especially in small animals or in animals with CSF flow obstruction at the level of the cerebellar cistern.

Most dogs with GME are small breeds, some of which are predisposed to craniocervical junctional malformations, such as Chiari type malformations.

I do not practice routine CSF sampling in dogs with a high likelihood of GME, especially those with neurological abnormalities suggestive of brain damage. CSF analysis is useful for evaluating animals with spinal cord or meningeal involvement (I usually use lumbar puncture).

It is also possible to identify changes characteristic of an inflammatory disease using visual methods for examining the brain; MRI is considered the treatment of choice for GME. Magnetic resonance imaging (MRI) is the most sensitive technology for visual diagnosis of diseases of the brain and spinal cord. MRI units with powerful magnets 1.0 T, 1.5 T allow better visualization of inflammatory lesions than units with weak magnets. However, there is no “typical” MRI pattern, and changes may be indistinguishable from those observed in infectious, vascular, or neoplastic diseases. Solitary or multiple lesions can be found in any part of the central nervous system, they can be hypointense on T1-weighted images and hyperintense on T2-weighted and FLAIR images. The degree of contrast enhancement varies. It is possible to increase the contrast of the meninges. However, the most typical multifocal lesion. Imaging also helps rule out other causes of brain or spinal cord involvement, such as neoplasms or vascular abnormalities, although focal granulomas in GME may show a pattern very similar to neoplasms and infarctions, as the inflammation sometimes looks very similar to vascular abnormalities from other causes.

With necrotizing encephalitis in Chihuahuas, pugs, Maltese lapdogs, etc., characteristic multiple foci are found in the cerebral hemispheres with an erased border between gray and white matter and areas of hyperintensity on T2-weighted / hypointensity on T1-weighted images corresponding to areas of necrosis.

In some cases of inflammatory diseases of the CNS, MRI does not show changes.

Computed tomography (CT) is less sensitive, especially when examining lesions in the caudal fossa (artifact of increased beam stiffness). Displacement of the falx medulla or change in its normal anatomy as a result of compression by a bulky neoplasm can be either visible or invisible on CT or MRI images.

The final diagnosis of GME is possible only on the basis of the results of histological examination of the brain - which is obviously difficult to do in vivo. Microscopically, GME is characterized by tissue infiltration along the vessels by lymphocytes and/or macrophages. Such foci may merge into granulomas, visible macroscopically.

A presumptive diagnosis of HME is often made by exclusion of other causes (by serology/CSF culture in some circumstances) and, in many cases, by treatment outcome. To exclude infectious causes of meningoencephalitis, serum can be tested to determine the titers of cryptococcal antigen, antibodies to toxoplasma gondii and neospora caninum (in some cases, CSF is also examined). CSF cultures are often negative, even with bacterial and fungal infections.

When an animal has severe neurological symptoms, the benefits of diagnostic testing, especially CSF, should be weighed against the risks of the procedure.

The causes of GME are unknown, but most likely it is an autoimmune process based on T-cell mediated hypersensitivity.

It's hard to make a prediction. GME can be an acute, rapidly progressive, and fatal disease despite treatment, but in many cases of suspected GME, treatment works well and animals remain in remission for months or years. In most published sources, the prognosis for GME is indicated as unfavorable or hopeless, but in practice there are cases of successful treatment. Since the diagnosis is based on the results of histological examination, the authors of published works usually rely on cases of confirmed diagnosis (i.e., post-mortem).

The prognosis does not depend on the severity of clinical symptoms at admission, as well as on the severity of changes in the analysis of CSF or imaging of the brain.

Corticosteroids (mainly prednisolone) in immunosuppressive doses remain the mainstay of treatment. In many cases (for financial reasons and/or due to the risk of further diagnostic tests) treatment is given empirically without further confirmation of the diagnosis.

Initial dose of prednisolone 1–2 mg/kg every 12 hours Small dogs (<12 кг) следует давать 2 мг/кг каждые 12 ч. Собакам с весом <2,5 кг следует давать такую же дозу, как для собак весом 2,5 кг, а с весом <5 кг – такую же, как для собак весом 5 кг. Доза для более крупных собак (>40 kg) corresponds to a dose for dogs weighing 40 kg, in general, I would not recommend giving more than 40 mg every 12 hours for a long time. Response to corticosteroid therapy may take several days.

The dose of prednisolone is gradually reduced over at least 6 months, depending on the clinical response. The first time the dose is reduced after 2-4 weeks. After achieving remission, a maintenance dose of prednisolone (0.5–1 mg/kg every other day or 2–3 times a week) is used for 1–2 years. It is difficult to establish whether an animal has “cured”. If a dog receiving low-dose prednisolone 2-3 times per week has no neurological symptoms for >6 months, treatment may be discontinued. However, the side effects of corticosteroids, especially in large dogs, can be a significant problem in the long term. Long-term use of corticosteroids leads to iatrogenic hyperadrenocorticism, accompanied by significant wasting of muscle mass and calcification of the skin. In addition, treatment predisposes to gastrointestinal ulceration, pancreatitis, diabetes mellitus, infections (especially of the urinary tract), and ligament and tendon injuries.

Small dogs often tolerate high doses well, but animals that experience a relapse of neurological symptoms while on corticosteroid therapy, require high doses of corticosteroids (>1 mg/kg) for long periods of time to relieve neurological symptoms, or have significant side effects should consider using other immunosuppressants.

For large dogs, timely supplementation is recommended because many animals do not tolerate high doses of corticosteroids. All dogs with severe neurologic impairment associated with spinal cord injury should receive additional therapy, such as cytarabine, early in treatment. The addition of other immunosuppressants can reduce the dose of prednisolone, but the need for a certain dose of prednisolone remains in most animals.

Azathioprine (Imuran) - an immunosuppressant that suppresses the function of T-cells. In healthy dogs, it does not cross the blood-brain barrier. While this drug may be effective in steroid-responsive meningitis, especially in young large breed dogs, it is not useful in GME in my opinion. However, other clinicians recommend imuran and describe successful use of azathioprine in combination with prednisolone, which allowed the dose of the latter to be reduced. This drug causes almost no side effects, the main problem at high doses is the suppression of bone marrow activity. The recommended dose is 0.5–1.0 mg/kg every 48 hours. For the first 5–7 days, it can be given at a dose of 2 mg/kg every 24 hours.

Cytosine arabinoside (cytarabine, ara-C) - a drug used as an antineoplastic agent for dogs and humans, for example, for the treatment of CNS lymphoma. Its mechanism of action is unknown. Since this drug crosses the blood-brain barrier and is an immunosuppressant, it was proposed approximately 6 years ago as a possible treatment for GME. Most authors recommend using it at a dose of 50 mg/m2 subcutaneously twice a day for 2 consecutive days, repeating this cycle every 3 weeks. This dose is lower than the usual dose for cancer chemotherapy. The number of side effects of cytarabine is small. Bone marrow suppression has been described (usually 10 to 14 days after the start of treatment), but this usually does not lead to clinical impairment. It is recommended to periodically do a complete blood count, but not necessarily at each cycle. After treatment, vomiting, diarrhea and/or loss of appetite may occur. Cytarabine is inexpensive (when purchased in 10 ml vials) and suitable for outpatient treatment, however, protective gloves must be worn when administering this drug and handling/disposing of urine and faeces. Cytarabine is used in combination with prednisolone; if the neurological status of the animal remains stable, I usually gradually reduce the dose of prednisolone every 2 cycles of cytarabine. Cytarabine can be used indefinitely.

Leflunomide (Arava) - an immunosuppressant, used in medicine mainly for the treatment of rheumatoid arthritis. Successful use in the treatment of dogs has been described, first in combination with corticosteroids, and then alone (for uncontrolled adverse reactions to corticosteroids). The initial dose is 2 mg/kg per day. In my practice, animals relapsed or did not improve. This drug does not cause any significant side effects and is given by mouth. Can be combined with prednisone.

Cyclosporine - has also been proposed for the treatment of GME due to the latter's presumed autoimmune T-cell nature. Cyclosporine is a powerful immunosuppressant that suppresses T-cell immune responses. In healthy animals, the permeability of the blood-brain barrier to cyclosporine is low. However, since HME occurs with damage to the tissues around the vessels and a possible violation of the blood-brain barrier, it is assumed that the concentration of cyclosporine in the affected areas of the CNS may be higher. My experience with this drug is limited, with two dogs failing to respond to prednisone and cytarabine therapy.

Procarbazine - an antitumor agent that is lipid soluble and easily penetrates the blood-brain barrier; It is mainly used in medicine for the treatment of lymphoma. A dose of 25–50 mg/m2 per day is recommended. Procarbazine often causes side effects, including bone marrow suppression (30%), hemorrhagic gastroenteritis (15%), nausea, vomiting, and liver dysfunction. I have no experience with this drug, and its effectiveness has not been proven. Side effects and low availability limit its use.

Lomustine (CCNU) - an antitumor alkylating drug of the nitrosourea class, highly soluble in lipids and penetrating the blood-brain barrier. Doses used to treat GME are relatively arbitrary, but high doses are not recommended. Treatment with lomustine has been associated with significant, in some cases life-threatening, bone marrow suppression, gastrointestinal ulceration, and hepatotoxicity. The frequency of side effects increases with increasing dose, but such effects sometimes occur at an initial relatively low dose. Sepsis is a significant risk factor for bone marrow suppression. Toxicity is unpredictable and I do not recommend routine use of this drug for primary treatment.

Seizures require anticonvulsants.

Sick animals should not be vaccinated unless absolutely necessary. Vaccination may lead to recurrence of clinical symptoms. In addition, a low-fat diet is recommended.

Response to therapy is usually assessed by the reduction or disappearance of clinical symptoms. Repeated analysis of CSF is usually not recommended, since the severity of changes (or their absence) weakly correlates with the severity of CNS inflammation.

In my experience, at least 60% of dogs with suspected GME or steroid-responsive noninfectious meningoencephalitis respond well to corticosteroid monotherapy and can eventually be phased out without further relapse. However, relapse may occur days, weeks, months, or years after the first onset of clinical signs. If neurologic symptoms persist despite high doses of corticosteroids and/or prednisolone, and if the dose is reduced<2 мг/кг в сутки после нескольких месяцев терапии наступает рецидив, долговременный прогноз менее благоприятный.

Animals that require high doses of corticosteroids for a long time to reduce neurological symptoms can be supplemented with cytarabine; this will reduce the dose of prednisolone and achieve an acceptable quality of life for several months and even >1 year.

Other types of idiopathic meningoencephalitis have been described in several small breeds, including pug encephalitis, necrotizing encephalitis of Yorkshire terriers (necrotizing leukoencephalitis), Chihuahuas, and Maltese lapdogs (necrotizing meningoencephalitis).

Necrotizing encephalitis is also found in other toy breeds.

Histological sections reveal extensive inflammation and predominant necrosis of the cerebral cortex. Often, these pedigree inflammatory diseases present with a pattern of necrosis and cavities in the brain parenchyma, with meningeal lesions may or may not be present, and changes on MRI scans closely match lesions found post-mortem. The prognosis in all such cases is very cautious.
Treatment is the same as for GME, although response to treatment is often poorer.

Inflammatory processes in the membranes of the brain are a serious pathology that requires immediate qualified assistance. Most often, meningitis has an infectious nature and manifests itself as a secondary disease. Therapeutic measures are aimed at eliminating the main cause of the disease. With an infectious form of the disease, antibacterial drugs are included in the therapy, with non-infectious ones, hormonal agents are used.

Read in this article

Reasons for the development of the disease

Veterinarians, based on many years of practice, the main causes of meningitis in dogs include the following:

  • Infectious diseases of a viral and bacterial nature. Inflammation of the meninges accompanies such severe infections as rabies, leptospirosis, canine distemper, malignant catarrhal fever, viral meningoencephalitis, pasteurellosis. Pathogenic microorganisms enter the membranes of the brain through the bloodstream, through the lymphatic system or through the neurogenic pathway, causing swelling and inflammation.

The factor provoking the disease is often a prolonged allergic reaction, hypothermia or heat stroke. A poorly developed immune system in puppies and a decrease in resistance in older animals often leads to the fact that any infection penetrates the meninges, leading to the development of a serious illness.

Varieties

Depending on the etiology of a severe illness, veterinary medicine distinguishes between infectious and non-infectious (aseptic) meningitis, as well as primary and secondary. The infectious form of the disease is caused by the introduction of viruses, bacteria, protozoa, pathogenic fungi, etc. into the meninges.

Aseptic meningitis develops, as a rule, against the background of the action of chemical toxins, poisons, and is also caused by autoimmune reactions of the body. The non-infectious form is often diagnosed in Bernese Mountain Dogs, Pugs and Beagles. Dogs of these breeds are prone to granulomatous meningitis, as well as a hormone-dependent form of the disease.

According to the localization of the pathological process, veterinary specialists distinguish between focal and cerebral meningitis. If the dura mater has undergone inflammation, then we are talking about pachymeningitis. In the case when inflammation has engulfed the arachnoid membrane, experts speak of arachnoiditis, and when the soft cerebral membrane is involved in the pathology, it is about leptomeningitis.

By the nature of the inflammatory process, a purulent and serous form of the disease is distinguished. Purulent meningitis develops, as a rule, when a bacterial infection penetrates the membranes. The serous form is characteristic of aseptic meningitis and inflammation caused by a non-infectious cause.

The primary form is observed in the absence of an infectious disease in the anamnesis. Secondary meningitis develops as a complication against the background of the main infectious disease.

Symptoms of meningitis in dogs

The owner can suspect a dangerous pathology in a four-legged pet by paying attention to the following clinical signs:


The inflammatory process is often accompanied by a disorder of the respiratory and cardiac activity. With untimely treatment, the death of a pet occurs due to paralysis of the vital centers of the brain responsible for breathing and heart rate.

Diagnostic methods

Given the danger of nervous pathology for the life of the animal, the owner should show the dog to a veterinarian as soon as possible. An accurate diagnosis in a short time can be established by equipping the clinic with high-tech equipment.

An informative research method is craniography (X-ray examination of the skull), magnetic resonance and computed tomography. With their help, the veterinarian will not only detect the inflammatory focus, but also assess its localization. Severe pathological changes are detected during an electroencephalogram.


CT of the brain in a dog with meningitis: A) GM before the introduction of a contrast agent; C) GM after intravenous administration of a contrast agent (arrows show inflamed areas of the GM, where the contrast agent has leaked through the blood vessels)

The analysis of cerebrospinal fluid allows to establish the infectious nature of meningitis and determine the type of pathogenic microorganism. For this purpose, an atlanto-occipital puncture is performed under general anesthesia. With meningitis, a pronounced lymphocytosis, neutrophilia are found in the cerebrospinal fluid, and the number of cells (pleocytosis) increases.

Additional diagnostic methods include clinical analysis of blood and urine, ultrasound and X-ray examination of the chest and abdominal organs. Differentiate meningitis from non-communicable diseases such as hydrocephalus, hypoglycemia,.

Treatment of meningitis

To treat the infectious form of the disease, antibacterial and antiviral drugs are used that have the ability to freely pass through the blood-brain barrier. In veterinary practice, for this purpose, sick pets are prescribed antibiotics of the penicillin and cephalosporin series (Ampicillin, Ampiox, Cefazolin, Cefotaxime).

Sulfonamides are used in the maximum dose. A good therapeutic effect in case of illness is the use of fluoroquinolones, for example, Enroxil, Marfloxin. The course of treatment is from 14 to 28 days, depending on the severity of the disease. Corticosteroid drugs help relieve inflammation - Prednisolone, Dexamethasone.

In the event that the viral nature of meningitis is confirmed, the sick pet is prescribed specific antiviral drugs - serum, gamma globulin. The use of non-specific agents is also effective - Interferon, Betaferon.

In addition to fighting inflammation, complex therapy includes the use of decongestants and painkillers. Mannitol, Furasemide, Dicarb help reduce cerebral edema. No-shpa, Spazgan help relieve pain.

In case of neurological symptoms, the animal is prescribed Cerebrolysin, Cocarboxylase. Reduces excitability and has a calming effect on the nervous system Phenobarbital, Diazepam.

In the treatment of the aseptic form of the disease, not only corticosteroids are successfully used, but also non-steroidal anti-inflammatory drugs, such as Ibufen.

Detoxification therapy includes intravenous injections of Gemodez, Poliglukin. It is useful to use intramuscular administration of B vitamins - thiamine, riboflavin, pyridoxine and ascorbic acid to maintain the normal functioning of the nervous system of a sick animal and restore brain metabolism.

About the causes, symptoms and treatment of meningitis in dogs, see this video:

Vaccination as a reliable method of prevention

Timely vaccination against major infections (leptospirosis, rabies, canine distemper, etc.) can protect a four-legged pet from a dangerous disease. Veterinary medicine has a wide arsenal of highly effective polyvalent vaccines that protect dogs from a variety of diseases accompanied by inflammation of the meninges.

Meningitis in dogs is a dangerous inflammatory process of the nerve sheaths of the brain. The disease often develops against the background of a primary infection (bacterial, viral, fungal). The complex therapy includes the use of antibacterial, decongestant, corticosteroid, painkillers, anticonvulsants. Given the high mortality rate, it is important to start adequate treatment of a sick dog in time.

is an inflammatory disease of the membranes of the brain and spinal cord.

Causes of occurrence.

According to the etiology, meningitis is divided into infectious and non-infectious.

According to the nature of the inflammatory process, serous and purulent, by localization on spinal and cerebral.

There are two forms of this disease primary and secondary meningitis. Primary meningitis develops if, when the body is infected, the disease immediately affects the brain (, Aujeszky's disease, viral,).

Aseptic meningitis includes steroid-dependent meningitis, granulomatous meningoencephalitis, pain syndrome, meningitis, meningoencephalitis. The causes of steroid-dependent meningitis are still not known, but due to the positive effect on steroid therapy, they are classified as autoimmune diseases.

Depending on the localization of the inflammatory process, focal and cerebral symptoms may develop.

General symptoms include:

Fever

Pain and stiffness of the muscles of the neck and forelimbs

Extreme sensitivity to touch (hypersthesia)

Loss of appetite

lethargy

Nausea, vomiting

Gait disturbance (becomes wobbly, the animal stumbles, tries to lift its legs high)

Inability to bend legs

Oppression

progressive paralysis

convulsions

Disorientation

Loss of coordination.

Aggression

Meningitis can be fatal. With damage to the medulla oblongata, death occurs from paralysis of the vascular-vegetative and respiratory centers.

Focal symptoms include:

Irregular pupillary dilation

Trembling of the eyeballs

Strabismus

Lowering of the upper eyelid and ear

Dropping of the lower jaw

The prognosis is cautious, often unfavorable.

If your dog shows any of these symptoms, you should immediately contact veterinary neurologist. Early diagnosis of meningitis is important for its successful treatment and recovery.

For the treatment of aseptic forms of meningitis, steroids are used, in most cases giving a positive effect.

Dogs suffering from seizures are given anticonvulsant therapy.

Other types of meningitis, including bacterial meningitis are more difficult to treat. To combat infectious agents, it is necessary to administer antibacterial drugs that can penetrate the blood-brain barrier and reach therapeutic concentrations in the cerebrospinal fluid.

Unfortunately, some dogs die despite treatment, while others make a full recovery. Early diagnosis and timely active treatment can greatly increase a dog's chances of recovery.

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