1. Bacterial
1.1. Streptococcal meningitis
1.1.1. Causative agent : Streptococcus pneumoniae
1.1.2. Virulence factor : The virulent strains are encapsulated
1.1.3. Mode of transmission: by direct contact (respirating droplets from nose and throat of infected people)
1.1.4. Signs and symptoms: Fever, drowsiness, stiff neck, vomiting
1.1.5. Pathogenesis: - The bacteria transmitted via direct contact thru the respiratory droplets from nose and throat of the infected person. - The bacteria will adhere and colonizes at nasopharynx. - When it enters the blood stream, the bacteria capsule will help pneumococcus to evade the opsonization. - The pneumococcus have the access to the CSF through the receptors on the endothelial surface of the blood-brain barrier and lead to the high fever, drowsiness, severe headche.
1.1.6. Preventions and treatments: post exposure passive and active immunization, euthanize (kill) all rabid animals, anti rabies vaccines
1.2. Meningococcal meningitis
1.3. Haemophilus meningitis
1.4. Listeriosis
1.4.1. Causative agent: Listeria monocytogenes
1.4.2. Virulence factor: can shed the cell walls
1.4.3. Mode of transmission: foodborne transmission
1.4.4. Signs and symptoms: infect fetus, abortion,neonatal death,fetal damage, inflammation of brain.
1.4.5. Pathogenesis: - The bacteria were transmitted by the contaminated food such as milk. - The bacteria then shed their cell wall to become L-forms. - L-forms can survive longer than normal forms which can be killed in 30 minutes by injection of phagocytes - This is because they are not indicate as pathogen and the bacteria can cross the placenta that can infect the fetus or lead to an abortion.
1.4.6. Preventions and treatments: wash the fruits or vegetables before eat,
1.5. Brain abscesses
1.5.1. Causative agent: various anaerobes
1.5.2. Mode of transmission: from head wound, via blood stream, infection of the body, surgery
1.5.3. Signs and symptoms: headache, fever, numbness, stiffness, seizures
1.5.4. Pathogenesis: - The microorganisms enters through the wound infection. - The microorganisms will form the brain abscess when it reach the brains. - It will cause infection that can gradually grow in mass and compress the brain. - That may lead to the severe headaches, fever, numbness.
1.5.5. Preventions and treatments: take antibiotics, surgical drainage or removal of abscess, glucocorticoid medication
2. Viral
2.1. Rabies
2.1.1. Causative agent: Rabies virus
2.1.2. Virulence factor: A single stranded RNA virus
2.1.3. Mode of transmission: through animal bite or break in the skin
2.1.4. Signs and symptoms: Fever, depression, agitation, painful spasm followed by excessive saliva
2.1.5. Pathogenesis: - The virus usually enters via rabid animal bite (dogs,bats) - When the virus enters, it will replicate in the muscle at the site of the bite. - Then, the virus will infect the nerve in the peripheral nervous system that moves by the retrograde transport. - The virus will replicate in the dorsal root ganglion and travels up to the spinal cord and towards brain. - The brain will be infected and the virus continues to travels from the brain via nerves to the other tissues such as eye, kidney,salivary glands.
2.1.6. Preventions and treatments: post exposure passive and active immunization, euthanize (kill) all rabid animals, anti rabies vaccines
2.2. Encephalitis
2.2.1. Causative agents: variety of togavirus or flavivirus
2.2.2. Mode of transmission: from mosquito
2.2.3. Signs and symptoms: fever,headache, convulsions
2.2.4. Pathogenesis: - The virus will enters the body through the bites of the infected mosquitoes - The virus then multiply in the skin and spread to the lymph nodes. - Viremia occurs as it involves large number of virus. - The virus then invade the central nervous system and cause shrinkage and neurons lysis.
2.2.5. Preventions and treatments: get vaccine, practice good hygiene, apply mosquito repellent, use insecticide
2.3. West Nile Fever
2.3.1. Causative agent: Arbovirus
2.3.2. Virulence factor: A positive single stranded RNA flavivirus
2.3.3. Mode of transmission: through mosquitoes
2.3.4. Signs and symptoms: high fever, headache, chills, fatigue, swollen lymph
2.3.5. Pathogenesis: - The virus usually infects thru the mosquitoes - The mosquitoes uninfected the bird (the host) - The virus amplifies within the birds and the uninfected mosquitoes will bites the bird make it infected - But the virus does not amplify well within humans and horse as they considered as dead-end hosts.
2.3.6. Preventions and treatments: clean the rabid bite animal with soap and large amount of water, take vaccine, immunize the pets, take pain relievers to reduce pain
2.4. Progressive multifocal leukoecephalopathy
2.4.1. Causative agent: Jc virus,polyomavirus
2.4.2. Mode of transmission: through respiratory or gastrointestinal tract.
2.4.3. Signs and symptoms: vision and speech impairment, limb paralysis, mental deterioration
2.4.4. Pathogenesis: - The virus usually enter through the respiratory or gastrointestinal tract. - The virus then replicate in the cells. - Viremia occurs and allow the virus to reach target organs such as kidneys, brain. - Then, the virus produces myelin which is a lipoprotein that coats nerve fibers in the central nervous systems and can infect the oligodendrocytes.
2.4.5. Preventions and treatments: do the reversal immune-deficient state,
3. Bacterial Nerve
3.1. Hansen’s Disease
3.1.1. Causative agent: Mycobacterium leprae
3.1.2. Virulence factor: contain mycolic acid in cell wall
3.1.3. Mode of transmission: through wound or infection
3.1.4. Signs and symptoms: numbness, depends on cell mediated immune
3.1.5. Pathogenesis: - The bacteria usually infects due to the invasion of small nerve of skin - Then, the bacteria will multiply in the macrophages and attack the immune cells against the infected nerve cell. - This can cause deformity.
3.1.6. Preventions and treatments: take depsone and rifampin for months or years and add clofazimine for lepromatous disease
3.2. Tetanus
3.2.1. Causative agent: Clostridium tetani
3.2.2. Virulence factor: - produce exotoxin known as tetanospasmin - can survive in environment that lack of oxygen
3.2.3. Mode of transmission: through wound, injury, infection
3.2.4. Signs and symptoms: muscle spasm, lockjaw, respiratory muscle paralyse, heart function disturb
3.2.5. Pathogenesis: - Anaerobic condition allow the germination of the spores and have a little inflammation at the infection site - The bacteria will produces exotoxin (tetanospasmin) that will bind to the ganglioside at the myoneural junction of skeletal muscle and on the neuronal membranes in the spinal cord that block the inhibitory impulses to motor neurones. - This can leads to the unopposed muscle contraction and spasm. The movement mimic the seizures.
3.2.6. Preventions and treatments: take tetanus toxoid vaccine, antibiotic for injured part, antitoxin for toxin inactivation
3.3. Botulism
3.3.1. Causative agent: Clostridium botulinum
3.3.2. Virulence factor: produce botulin toxins
3.3.3. Mode of transmission: spores, widespread in soil, contaminated vegetables and meats, canned food not sterile
3.3.4. Signs and symptoms: double vision, droopy eyelids, trouble speaking,swallowing or breathing, muscle weakness
3.3.5. Pathogenesis: - The bacteria usually can be transmitted by contaminated vegetables and meats. - When the bacteria enters, it will produce toxins that is absorbed to the blood stream. - It will leaves the circulatory system at the point where the neuron join the muscle. - The toxin produced will prevents the fusion of synaptic vesicles of the acetylcholine. - The paralysis of the muscle fiber will occur due to the no release of the acetylcholine at the neuromuscular junction.
3.3.6. Preventions and treatments: treated with botulism antitoxin, remove contaminated food in digestive tract by vomiting or using enemas
4. Viral Nerve
4.1. Poliomyelitis
4.1.1. Causative agent: Poliovirus
4.1.2. Virulence factor: have a icosahedral capsid shell that can protects from digestion
4.1.3. Mode of transmission: spread from person to person through infected fecal matter entering the mouth, spread by food or water containing human feces
4.1.4. Signs and symptoms: loss of reflexes, severe muscle aches, weakness, loose and floppy limbs( flaccid paralysis)
4.1.5. Pathogenesis: - The virus usually spread from person to person through infected fecal matter that enters the mouth. - Then, the virus will travels through the blood, nerves and places in the cord where the nerve cell are destroyed. - This lead to the paralysis of the part of the body controlled by the motor neurons. - Then, the virus will multiply in the motor neurons that mainly in the anterior horn cells. - The virus also may affect the brainstem.
4.1.6. Preventions and treatments: immunization with inactivated polio vaccine, do the physical treatment
5. Virulence factors: produce myelin
6. Prion
6.1. Transmissible spongiform encephalopathies
6.1.1. Causative agent: prions
6.1.2. Virulence factors: lack of inflammatory response
6.1.3. Mode of transmission: breaks in skin
6.1.4. Signs and symptoms: create spongiform brain tissues, spasms rapidly worsening, brain cells die long delay before symptoms appear
6.1.5. Pathogenesis: - The prions enter the body through the breaks in skin. - The prions then inoculate in the cells and lead to headache, minor loss of coordination. - The prions will make the brain cells die and cause a spongiform brain tissue and make the amyloid plaques accumulate. - The symptoms usually begin with spasm that rapidly worsen to collapse and followed by death.
6.1.6. Preventions and treatments: no treatments available
7. Parasite
7.1. African Sleeping Disease
7.1.1. Causative agents: Trypanosoma sp.
7.1.2. Virulence factor: have an undulate membranes
7.1.3. Mode of transmission: through the bite of infected tsetse fly
7.1.4. Signs and symptoms: shortness of breath, cardiac pain, anemia, headache, stiffness
7.1.5. Pathogenesis: - The parasites enter the body thru the bites of the tsetse flies. - The inflammatory reactions occur. - When the parasites appear in the blood, fever will occurs. - The patient can survive for the first and second stage but when the parasites invade the nervous system, it can cause tremors, headache. - If the disease progress, it can lead to death.
7.1.6. Preventions and treatments: take pentamidine, suramin, apply aerial pesticides, clear brush where flies congregate
7.2. Chagas’ Diseases
7.2.1. Causative agent: Trypanosoma cruzi
7.2.2. Virulence factor: deactivate T cells
7.2.3. Mode of transmission: thru the several kinds reduviid bugs
7.2.4. Signs and symptoms: muscle pain, paralysis, subcutaneous inflammation, nervous disorder
7.2.5. Pathogenesis: - The disease will begins with the subcutaneous inflammation around the bug bite - The parasites will divide and form aggregates known as pseudocysts after 1 or 2 weeks. - The pseudocysts will rupture make an inflammation and tissue necrosis occurs. - The parasites the will enter the cell via invasion or phagocytosis and cause damage at lymphatic tissues, all kinds of muscle especially the supporting tissues around the ganglia nerve. - The destruction of the ganglia nerve will lead to the death from heart disease in the endemic areas.
7.2.6. Preventions and treatments: use insecticide, no treatments available,