RABIES

 

INTRODUCTION: No sound invokes more terror in mankind than the bark of a rabid dog. It has terrified man since time immemorial. The fear by no means is unfounded because the disease transmitted by such animal in humans is perhaps the most painful and horrible of all the communicable diseases in which the sick person is tormented with thirst and the fear of water a condition known as hydrophobia, at the same time.

CLASSIFICATION: Rabies virus belongs to the family Rhabdoviridae and genus Lyssavirus which contains four related but distinct virus types.

MORPHOLOGY: The rabies virus is bullet shaped, round at one end and flat at the other. Though the dimensions vary, it ranges between 200 × 80 nm. The membrane at the flattened end of the virion often appears invaginated. Atypical elongated filaments and occasional Vor Y-shaped and conical forms are observed in rabies virus harvested from cell cultures late after infection. Truncated bullets (T-particles) encountered in many rhabdovirus preparations are non-infectious.

CHEMICAL COMPOSITION: The RNA is an unsegmented, single, negative strand which is non-infectious. The RNA is closely associated with a major protein, N and two smaller proteins, L and NS. This structure is tightly coiled and helical in appearance and constitutes the nucleocapsid of the virus. It is enveloped in a lipoprotein membrane through which protrude a large number of spikes with knobs at their distal ends. The inner surface of the envelope is lined by a genome coded M protein. Associated with the envelope is a glycoprotein (G) of which the surface projections are composed.

SUSCEPTIBILITY TO PHYSICAL AND CHEMICAL AGENTS: The rabies virus is highly resistant to cold, dryness, decay, etc. It can remain infectious for weeks in the cadavers. Rabies virus is thermolabile, with a half life of approximately 4 hours at 40°C and 35 seconds at 60°C. However, thermal inactivation is diminished in the presence of serum proteins and chelating agents. The virus remains stable for several days at 0-4°C, indefinitely at –70°C and when freeze dried. This virus cannot withstand pH less than 4 or more than 10. It is also susceptible to the action of oxidising agents, most organic solvents, surface acting agents, quaternary ammonium agents, soaps and detergents. Proteolytic enzymes, ultraviolet rays and X-rays rapidly inactivate rabies virus.

STREET AND FIXED VIRUS STRAINS: The street virus which was first designated by Pasteur as virus des rues refers to the virus isolated from animals and which has not undergone any modification in the laboratory. The strains of this type are characterised by a variable incubation period and by their capacity to invade salivary glands. The fixed virus, by contrast, refers to strains adapted to laboratory animals by serial intracerebral passages which have a short incubation period of only 4-6 days and do not invade the salivary glands. Fixed virus remains neurotropic and its virulence for the central nervous system may get enhanced; it produces paralytic rather than furious symptoms. Its infectivity by peripheral inoculation is diminished, as its ability to induce inclusion bodies in the central nervous system.

PATHOGENESIS: Compared to other mammals man is somewhat less susceptible to the rabies virus. However, the probability of contagion depends on the virulence of the particular virus strain, the quantity of virus transmitted by the bite and location of the bite. Whereas a bite on the face has a contagion index of almost 100% that on the body or leg only about 2%. Once the disease is established there is no cure. After a bite on the human body the neurotropic virus spreads mainly along the endoneural lymphatic ducts, thus reaching the brain and the spinal cord where it multiplies intracytoplasmically in the grey matter. The movement of the virus from peripheral sites to the CNS is effected by passive transport. The rate of movement for some strains has been estimated to be 3 mm/hour. Extensive replication occurs within the brain and terminally neurons in all the parts may be affected.

The symptomatology in cases with rabies is dependent upon the parts of brain affected. Pronounced localisation of virus in limbic system is responsible for furious and aggressive behaviour. Man to man transmission of rabies does not take place but corneal transplants from donors with undiagnosed rabies provide bizarre examples of human to human transmission.

CLINICAL FEATURES: The average incubation period is 30-90 days. It is shorter in case the bite is closer to brain. In a typical course of the disease, the uncharacteristic prodromal stage is followed by the excitation stage with high motor activity, tremors, tonic clonic spasms, opisthotonus, increased salivation, shortness of breath among others. The sight of water, sudden exposure to bright light or loud noise or subjecting him to a current of fast air, trigger violent spasms of the gullet making it impossible for the patient to drink water and hence the name hydrophobia. Unless prolonged by intensive care, disease progresses to coma and death ensues within 3-7 days after its onset. Aggression, delirium and intolerance to stimuli are among the behavioural changes frequently seen in patients with rabies. Hydrophobia does not manifest in all the cases but if present, leaves no doubt about the diagnosis. Death in rabies is usually due to respiratory paralysis while the patient is fully conscious.

RELATED;

1.  MUMPS VIRUS  

2.  EBOLA VIRUS

3.  MICROBIOLOGY

REFERENCES

SALMONELLA (GASTROENTERITIS, TYPHOID FEVER, PARATYPHOID FEVER)

 

INTRODUCTION: All salmonellae are classified in the species Salmonella enterica with seven subspecies. Nearly all human pathogen salmonellae are grouped under S. enterica, subsp. enterica. Salmonellae are further subclassified in over 2000 serovars based on their O and H antigens, which used to be designated as species. Typhoid salmonelloses are caused by the serovars typhi and paratyphi A, B, and C.

MODES OF TRANSMISSION: The salmonellae are taken up orally and the invasion pathway is through the intestinal tract, from where they enter lymphatic tissue, first spreading lymphogenously, then hematogenously. A generalized septic clinical picture results. Human carriers are the only source of infection. Transmission is either direct by smear infection or indirect via food and drinking water.  Anti-infective agents are required for therapy including but not limited to; ampicillin, cotrimoxazole, 4-quinolones). An active vaccine is available to protect against typhoid fever. Enteric salmonelloses develop when pathogens are taken up with food. The primary infection source is usually livestock. These relatively frequent infections remain restricted to the gastrointestinal tract. Treatment with antiinfective agents is necessary in exceptional cases only.  It is not known why typhoid salmonellae only cause systemic disease in humans, whereas enteric salmonella infections occur in animals as well and are usually restricted to the intestinal tract.

DIAGNOSIS: The method of choice is detection of the pathogens in cultures. Selective indicator mediums are used to isolate salmonellae in stool. Identification is done using metabolic patterns. Serovar classification is determined with specific antisera in the slide agglutination test. Culturing requires at least two days. Typhoid salmonelloses can be diagnosed indirectly by measuring the titer of agglutinating antibodies to O and H antigens (according to Gruber-Widal). To provide conclusive proof the titer must rise by at least fourfold from blood sampled at disease onset to a sample taken at least one week later.

THERAPY: Typhoid salmonelloses must be treated with anti-infective agents, whereas symptomatic treatment will suffice for enteric infections. Symptomatic treatment encompasses slowing down intestinal activity (e.g., with loperamide) and replacing fluid and electrolyte losses orally as required. Eliminating the infection in chronic stool carriers of typhoid salmonellae, 2–5% of cases, presents a problem. Chronic carriers are defined as convalescents who are still eliminating pathogens three months after the end of the manifest illness. The organisms usually persist in the scarified wall of the gallbladder. Success is sometimes achieved with high-dose administration of anti-infective agents, e.g., 4-quinolones or aminopenicillins.

PREVENTION: The main method of effective prevention is to avoid exposure: this means clean drinking water, prevention of food contamination, avoidance of uncooked foods in countries where salmonellae occur frequently, disinfection of excreta containing salmonellae or from chronic carriers, etc. It is also important to report all cases to health authorities so that appropriate measures can be taken.

RELATED;

1.  BRUCELLA  

2.  GRAM NEGATIVE ENTERIC BACTERIA

3.  BACTERIOLOGY

4. MEDICAL MICROBIOLOGY

REFERENCES