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- 1. CNS INFECTIONS Meningitis Inflammation of the brain and spinal cord that may be caused by either bacterial or viral infection. Bacterial meningitis=> Serious infection that is spread by direct contact with discharge from the respiratory tract of an infected person. Viral meningitis=> Also called aseptic meningitis, is more common and rarely serious. It usually presents with flulike symptoms and patients recover in 1 to 2 weeks 02/10/2023 1
- 2. Pathophysiology and Etiology Common bacteria causing meningitis: Neisseria meningitidis=> Meningococcal meningitis Streptococcus pneumoniae => Pneumococcal meningitis Haemophilus influenzae type b (Hib). N. meningitides and S. pneumoniae are the major causes of bacterial meningitis. Infection generally begins in another area, such as the URT enters the blood and invades the CNS causing the meninges to become inflamed and ICP to increase. 02/10/2023 2
- 3. Cont’d 02/10/2023 3 Necrosis of areas in the brain may occur. Cranial nerve function may be transiently or permanently affected by meningitis.
- 5. Signs and Symptoms The most common symptom of meningitis is Headache High grade fever and stiff neck Photophobia Patient with meningococcal meningitis usually presents with petechiae on the skin and mucous membranes. Nuchal rigidity (pain and stiffness when the neck is moved) is caused by spasm of the extensor muscles of the neck. Positive Kernig’s and Brudzinski’s signs 02/10/2023 5
- 6. Cont’d Kernig’s sign, the examiner flexes the patient’s hip to 90 degrees and tries to extend the patient’s knee and positive if the patient experiences pain and spasm of the hamstring. Brudzinski’s sign is positive when flexion of the patient’s neck causes the hips and knees to flex Nausea and vomiting associated 02/10/2023 6
- 7. Cont’d Encephalopathy =mental status changes manifested as : Short attention span, poor memory, disorientation, difficulty following commands and misinterpret environmental stimuli Late signs of meningitis include lethargy and seizures 02/10/2023 7
- 8. Diagnostic Tests A lumbar puncture Viral meningitis Clear CSF with normal glucose level and normal or slightly increased protein level. No bacteria are seen, but the WBC count is usually increased. Bacterial meningitis CSF is turbid, or cloudy, because of the massive number of WBC and lowering glucose level. Bacteria are identified by Gram stain and culture Elevated protein in CSF. MRI or CT scan:- may be done to evaluate for complications 02/10/2023 8
- 9. Management Meningitis can be fatal if not promptly treated. Antibiotics are administered for bacterial meningitis. Antipyretics and a cooling blanket may also be used. Care should be taken to avoid cooling the patient too much because shivering increases the metabolic demand for oxygen and glucose. A quiet, dark environment lessens the stimulation to a patient who has a headache or photophobia and who may be agitated, disoriented, or at risk for seizures 02/10/2023 9
- 10. Cont’d Analgesics are given to lessen head and neck pain. Corticosteroid's and anti-inflammatory Antiemetic medications. The patient with meningococcal meningitis should be placed in isolation because this disease can be transmitted to others. 02/10/2023 10
- 11. Cont’d Nursing Management Maintain fluid balance (input and output) Maintain body temperature to normal Agitated patients, keeping patients from harming themselves. Teach the family about symptoms and treatment goals for the patient. Monitor vital signs 02/10/2023 11
- 12. Complications o Cranial nerve damage may leave the patient blind or deaf. o Seizures may continue to occur even after the acute phase of the illness has passed. o Cognitive deficits ranging from memory impairment to profound learning disabilities may occur 02/10/2023 12
- 13. Rabies Preventable viral disease most often transmitted through the bite of a rabid animal. Rabies virus infects the CNS of mammals, ultimately causing disease in the brain and death. Rabies Virus Rabies virus belongs to the order Mononegavirales – Within this group, viruses with a distinct “bullet” shape are classified in the Rhabdoviridae family, which includes Lyssavirus, – The genus Lyssavirus includes rabies virus 02/10/2023 13
- 14. Cont’d How is rabies transmitted? Transmitted through direct contact (such as through broken skin or mucous membranes in the eyes, nose, or mouth) with saliva or brain/nervous system tissue from an infected animal. People usually get rabies from the bite of a rabid animal. Possible, but rare for people to get rabies from non-bite exposures include: Scratches, abrasions, or open wounds that are exposed to saliva from a rabid animal. 02/10/2023 14
- 15. Cont’d Rabies virus becomes non-infectious when it dries out and when it is exposed to sunlight. If the material containing the virus is dry, the virus can be considered non-infectious. 02/10/2023 15
- 16. Pathophysiology Rabies virus is introduced into a muscle through a bite from another animal, it travels from the site of the bite to the brain by moving within nerves. The Person does not appear ill during this time. A bite by the animal during the incubation period does not carry a risk of rabies because the virus has not yet made it to the saliva. 02/10/2023 16
- 17. Cont’d The Infectious Path of the Rabies Virus 1. Person is bitten by a rabid animal. 2. Rabies virus from the infected saliva enters the wound. 3. Rabies virus travels through the nerves to the spinal cord and brain. This process can last approximately 3 to 12 weeks. The Person has no signs of illness during this time. 4. In the brain the virus multiplies rapidly and passes to the salivary glands. The Person begins to show signs of the disease. 5. The infected Person usually dies within 7 days of becoming sick. 02/10/2023 17
- 18. Sign and Symptom The first symptoms of rabies may be very similar to those of the flu including – General weakness or discomfort. – Fever or headache. These symptoms may last for days. There may be also discomfort or a irritation or itching sensation at the site of the bite progressing within days to acute symptoms of cerebral dysfunction Anxiety Confusion and agitation. 02/10/2023 18
- 19. Cont’d As the disease progresses the person may experience: Delirium Abnormal behaviour Hallucinations Hydrophobia (fear of water) and insomnia. Acute period of disease typically ends after 2 to 10 days. Once clinical signs of rabies appear the disease is nearly always fatal and treatment is typically supportive. 02/10/2023 19
- 20. Diagnosis Several tests are necessary to diagnose rabies ante-mortem (before death) in humans; no single test is sufficient. Saliva test by virus isolation or reverse transcription followed by polymerase chain reaction (RT-PCR). Serum and spinal fluid are tested for antibodies to rabies virus. Skin biopsy specimens are examined for rabies antigen in the cutaneous nerves at the base of hair follicles. 02/10/2023 20
- 21. Management Extensive wound washing This first-aid measure includes immediate and thorough flushing and washing of the wound for a minimum of 15 minutes with soap and water, detergent, povidone iodine or other substances that remove and kill the rabies virus. Post-exposure Prophylaxis (PEP) Dose of human rabies immune globulin (HRIG) and rabies vaccine given on the day of the rabies exposure and then a dose of vaccine given again on days 3, 7, and 14. 02/10/2023 21
- 22. Exposure risk and indications for PEP Categories of contact with suspect rabid animal Post-exposure prophylaxis measures Category I - touching or feeding animals, animal licks on intact skin (no exposure) Washing of exposed skin surfaces, no PEP Category II - nibbling of uncovered skin, minor scratches or abrasions without bleeding (exposure) Wound washing and immediate vaccination Category III - single or multiple transdermal bites or scratches, contamination of mucous membrane or broken skin with saliva from animal licks, exposures due to direct contact with bats (severe exposure) Wound washing, immediate vaccination and administration of rabies immunoglobulin 02/10/2023 22 WHO recommendation for administration of a full PEP depending on the severity of the contact with the suspected rabid animal
- 23. Tetanus (Lockjaw) Serious bacterial infection that affects the nervous system and causes muscles throughout the body to tighten. Also called lockjaw because the infection often causes muscle contractions in the jaw and neck. It can be life-threatening without treatment. Approximately 10 - 20 % of tetanus infections are fatal, according to the CDC 02/10/2023 23
- 24. Causes/Etiology Bacteria => Clostridium tetani. Spores can be found in dust, dirt and animal droppings. Spores are small reproductive bodies produced by certain organisms. Are often resistant to harsh environmental conditions, such as high heat. Person become infected when these spores enter the bloodstream through a cut or deep wound and bacterial spores then spread to the CNS and produce a toxin called tetano-spasmin. Toxin (poison) blocks the nerve signals from spinal cord to muscles. This can lead to severe muscle spasms. 02/10/2023 24
- 25. Cont’d Tetanus infection has been associated with: Crush injuries Injuries with dead tissue Burns Puncture wounds from piercings, injury (such as stepping on a nail) Wounds contaminated with dirt, feces or saliva Less commonly, it’s been associated with: Animal bites Dental infections Insect bites Chronic sores and infections 02/10/2023 25
- 26. Clinical manifestation Difficulty swallowing Spasms and stiffness in various muscles, especially those in jaw, abdomen, chest, back, and neck. Other common tetanus symptoms are: – Fast heart rate – Fever – Sweating – High blood pressure Incubation period —is between 3 and 21 days. Symptoms typically appear within 14 days trusted Source of initial infection. Infections that occur faster after exposure are typically more severe and have a worse prognosis. 02/10/2023 26
- 27. Diagnoses History and physical examination Sustained spasm of the facial muscles in which the person appears to be grinning, or painful muscular contractions. History of injury or wound No lab investigation for the tetanus 02/10/2023 27
- 28. Management Treatment depends on the severity of symptoms. Antibiotics such as penicillin to kill the bacteria Tetanus anti-toxoid (TAT)=10,000–20,000 IU IM as a single or tetanus immune globulin (TIG)= 3000–5000 IU of TIG as a single IM to neutralize the toxins that the bacteria have created in body Muscle relaxers to control muscle spasms Cleaning the wound to get rid of the source of the bacteria Difficulty of swallowing and breathing need a feeding tube or ventilator In some cases, a surgical procedure called debridement is used to remove dead or infected tissue. 02/10/2023 28
- 29. Complications o Breathing problems due to spasms of the vocal cords (laryngospasm) and spasms of the muscles that control breathing o Pneumonia (an infection of the lungs) o Brain damage due to lack of oxygen o Abnormal heart rhythm o Bone fractures and fractures of the spine due to muscle spasms and convulsions o Secondary infections due to prolonged hospital stays 02/10/2023 29
- 30. Poliomyelitis Is an acute viral infection of the nervous system caused by poliovirus types 1, 2 and 3. It is public health importance lies in the ability of polioviruses to cause permanent paralysis and sometimes death. It is readily transmitted, causing both endemic and epidemic disease. 02/10/2023 30
- 31. Cont’d Suggested case definition Possible: Acute flaccid paralysis(AFP) without other apparent cause. Probable: AFP with decreased /absent tendon reflexes, without other identified cause and with out sensory or cognitive loss. Confirmed: Serological evidence or isolation of virus, together with clinically compatible illness 02/10/2023 31
- 32. Cont’d Transmission Polio is spread by the faeco–oral route. Human being is the only reservoir. Long-term carriage does not occur. Poor hygiene favours spread 02/10/2023 32
- 33. Clinical features Most cases of polio are asymptomatic or present with a sore throat or diarrhoea. Paralysis is relatively rare: The proportion of paralytic cases increases with age from about 1 in 1000 in infants to 1 in 10 in adults. Post-polio syndrome may develop 10–40 years after recovery from an initial paralytic attack and Is characterised by further weakening of previously affected muscles. 02/10/2023 33
- 34. Cont’d Poliomyelitis should be considered in any patient with AFP with a history of recent travel to an endemic area. Vaccine-associated polio should be considered in a recently vaccinated individual with AFP (particularly after the first dose) or in a close contact of a recently vaccinated individual. Main differential diagnosis is GBS The paralysis in polio is usually asymmetric, whereas in GBS it is usually symmetrical. There is always residual paralysis in polio, whereas patients with GBS usually recover completely. 02/10/2023 34
- 35. Diagnoses Stool culture to identify polio virus. Poliovirus can be recovered from faeces for up to 6 weeks and in nasopharyngeal secretions for up to 1 week from onset of paralysis. At least two stool samples, 24 hours apart, should be obtained within 7 days of the onset of paralysis. Serological or by CSF examination N:B:-All cases of AFP should be investigated to exclude polio. 02/10/2023 35
- 36. Management Isolate the patient Fever, headache, back, and neck and muscle pain are relieved by using pain relievers and muscle relaxant medications. Usually NSAIDs like Ibuprofen, Diclofenac and Acetaminofen are preferred. Artificial ventilator for respiratory muscle paralysis Antibiotics for prevention of UTI, Pneumonia Bethanechol or urinary catheter for urine retention Positioning Physiotherapy 02/10/2023 36
- 37. Response to a case or cluster Immediate notification, by telephone to the CDC and to the regional and national epidemiologist. Request urgent stool virology. Treat a single case of indigenous wild polio as a national public health emergency. If confirmed, mass vaccination with OPV would be required, possibly at the national or subnational level. In the event of an outbreak, involve international agencies such as WHO. For an imported case, notify WHO or relevant national surveillance unit. For vaccine-associated cases, no specific action is required, although it may be an opportunity to review vaccine coverage locally 02/10/2023 37
- 38. ANTHRAX Caused by the spore-forming bacterium Bacillus anthracis. Is found worldwide in soil. Animals become infected through grazing in contaminated areas. Under natural conditions, humans contract the disease after close contact with infected animals or contaminated animal products such as hides, wool or meat. 02/10/2023 38
- 39. Classification and Epidemiology Has three clinical forms in humans: Inhalational Cutaneous and Gastrointestinal. Cutaneous anthrax Is the most likely way to develop anthrax. Results from inoculation of spores subcutaneously through a cut or abrasion. Gastrointestinal and oro-pharyngeal anthrax Occur in rural parts of the world where anthrax is endemic. Result from ingestion of meat contaminated with spores. 02/10/2023 39
- 40. Cont’d Cutaneous Anthrax – Primary lesion appears as a nondescript, painless, pruritic papule, usually on an exposed area such as the face, head, neck, or upper extremity. – Papule enlarges and develops a central vesicle or bulla with surrounding brawny, non-pitting edema. – Central vesicle enlarges and ulcerates over 1 to 2 days, becoming hemorrhagic, depressed, and necrotic and leading to a central black eschar. – Satellite vesicles may be present. – The eschar dries and falls off over the next 1 to 2 weeks. – Tender regional lymphadenopathy, fever, chills, and fatigue may occur. – Systemic disease has been reported to have a mortality of 20% if untreated. 02/10/2023 40
- 42. Cont’d INHALATIONAL ANTHRAX Clinical presentation and diagnosis. C/M develop rapidly after germination of anthrax spores. Incubation period = 1 to 6 days but may be prolonged by antibiotic administration. Described as a two-stage disease. Initial stage Nonspecific, flulike illness lasting from several hours to a few days. Early clinical presentation includes: some combination of fever, myalgia, headache, cough, mild chest discomfort, weakness, abdominal pain, and chest pain. 02/10/2023 42
- 43. Cont’d Profound malaise, fever, and drenching sweats are prominent symptoms, and nausea and vomiting are frequent. Classically, the initial stage is followed 1 to 3 days later, sometimes after brief improvement, by the rapidly progressive second stage Second stage Characterized by fever, dyspnea, diaphoresis, cyanosis, and shock. 02/10/2023 43
- 44. Diagnosis There is no rapid screening test to diagnose inhalational anthrax in its early stages. Chest x-ray or CT scan, or both, and Culture and smear of peripheral blood. Pleural fluid and cerebrospinal fluid, as well as Biopsy specimens taken from the pleura and lung, are also potentially useful for culture and other testing when disease is present in these sites, Sputum culture and Gram stain are unlikely to be useful. 02/10/2023 44
- 45. THERAPEUTIC INTERVENTION. • Early IV antibiotic treatment may improve survival in inhalational anthrax. • Aggressive supportive care including: Attention to fluid, electrolyte, and acid-base disturbances Drainage of pleural effusions, also play an important role in treatment. • At present, intravenous ciprofloxacin or doxycycline plus one or two additional antimicrobials are recommended. 02/10/2023 45
- 46. INFECTION CONTROL Person-to-person transmission of anthrax is not known to occur. Patients may be hospitalized in a standard hospital room with standard barrier isolation precautions. No treatment is necessary for contacts of cases. 02/10/2023 46
- 47. TOXOPLASMOSIS Caused by Toxoplasma gondii – Protozoan parasite that causes a spectrum of disease from asymptomatic lymphadenopathy to congenital mental retardation, chorio-retinitis and encephalitis in the immuno-compromised. Epidemiology o Human exposure to toxoplasmosis is worldwide and common. o 20%-40% of healthy adults in developed countries are seropositive. o It is more common in Mediterranean countries than in Northern Europe. 02/10/2023 47
- 48. Clinical features Acute infection is usually asymptomatic, but may produce a mononucleosis-like illness. Congenital infection may occur following acute infection during pregnancy. Congenital toxoplasmosis is characterised by foetal hepato- splenomegaly, chorioretinitis and mental retardation. In the immuno-compromised, cerebral reactivation of toxoplasmosis may occur, with presentation as encephalitis. 02/10/2023 48
- 49. Laboratory confirmation Acute toxoplasmosis may be diagnosed serologically. – Specific IgM antibodies appear during the first 2 weeks, peak within 4–8 weeks, and then typically become undetectable within several months. – IgG antibodies rise more slowly, peak in 1–2 months, and may remain high for years. – Congenital infection requires the demonstration of IgM in neonatal blood; evidence of acute infection during pregnancy indicates the need for foetal blood sampling at 18 weeks and cord blood at delivery 02/10/2023 49
- 50. Cont’d • Serology is not useful for diagnosis of toxoplasmosis in patients with AIDS. • Cerebral toxoplasmosis is usually diagnosed on the basis of clinical features, a positive agglutination test and CT/MRI scan appearance. • Specific diagnosis in patients with AIDS and CNS symptoms requires a brain biopsy. 02/10/2023 50
- 51. Transmission The cat is the definitive host and transmits the infection through faecal shedding of oocysts. Children may come into contact with oocysts from pets, soil or sandpits. Adults are usually infected by ingestion of undercooked meat. Congenital infection usually occurs following primary infection in a pregnant woman. 02/10/2023 51
- 52. Pathogenesis – The incubation period is 10–25 days. There is no person-to-person spread. Prevention Pregnant women in particular should avoid raw or undercooked meat. Contact with soil or food possibly contaminated with cat faeces should be avoided. Chemoprophylaxis has been recommended for AIDS patients with positive IgG serology once CD4 cells are low. Protect sandpits and play areas from cats. 02/10/2023 52
- 53. Reference Linda s. Williams, paula d. Hopper (2007) Understanding medical surgical 3rd Edition Suzanne C. O’Connell Smeltzer, & Brenda G. Bare. (2010). Brunner and Suddarth’s Text Book of Medical-Surgical Nursing. 12th Edition. Lewis,M.S.,Heitkemper,M.M.,and Dirksen, S.(2000). Medical Surgical Nursing :Assessment And Management Of Clinical Problems .5th Ed. Kasper L, Braunwald el al.(2015). Harrison’s princeples of internal medicine,19th Edition. Mulugeta Alemayehu, CDC lecture note for nursing student, Hawasa university Jeremy.H, Norman .B et al.(2005). Communicable Disease Control Handbook ,2nd editon 02/10/2023 53