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Opportunistic Central Nervous System Infections John H. Samies, MD, FSHEA, CWS Infectious Diseases / Internal Medicine January 31, 2012 Overview • • • • • Define opportunistic infectious agents of the CNS Define high risk circumstances & populations Discuss pathogenesis of infectious agents Illustrate diagnostic approach & differential determination Describe some associated management issues Variety of organisms cause CNS infection This is all about • THE LOCATION • THE HOST • THE SETTING Location , location, location By Location – Meningitis: Inflammation of the meninges-the surrounding 3-layered membranes of the brain and spinal cord, and cerebrospinal fluid (CSF). – Encephalitis: Inflammation of the brain itself. – Myelitis: Spinal cord inflammation. – Abscess: Accumulation of infectious material and microorganisms within the CNS. Meningitis ENCEPHALITIS MYELITIS ABSCESS The host The Host • Opportunistic implies a loss of normal defense • An intact defense system is a complex interplay of protecting surfaces, cells and soluble factors. • The resident flora does not normally alert the immune system or cause disease – In fact may be protective • Ex : Meningococcus ( Neisseria meningitidis ) Risk factors for meningitis include : • • • • • • Age >60 years or < 5 years Diabetes mellitus, renal or adrenal insufficiency, hypoparathyroidism, or cystic fibrosis Immunosuppressive meds Human immunodeficiency virus Crowding (eg, military recruits and college dorm residents), Splenectomy (either surgical or due to splenic disease such as infarction ) and sickle cell anemia , which increase the risk of meningitis secondary to encapsulated organisms • • • • • • • • • • Alcoholism and cirrhosis Recent exposure to patients with meningitis, Contiguous infection (eg, sinusitis or mastoiditis) Dural defect (eg, traumatic, surgical, congenital) Thalassemia major Injecting (IV) drug use Bacterial endocarditis Ventriculoperitoneal shunt Malignancy (increased risk of Listeria species infection) Some cranial congenital deformities Loss of defense • Related to sheer number of pathogens • Related to breakdown of normal host – Alteration of resident flora – Alteration of integumentary protection • Skin / mucosa – Cellular dysfunction • Granulocyte • Lymphocyte • Monocyte/ macrophage – Humoral immune dysfunction B-lymphocyte dysfunction • Patients with disorders that decrease Blymphocyte function are particularly susceptible to meningitis caused by encapsulated bacterial pathogens. (Pneumococcus , Meningococcus ) • The presentation of bacterial meningitis is essentially the same in normal and compromised hosts with impaired Blymphocyte immunity. T-lymphocyte & macrophage dysfunction • Compromised hosts with impaired T-lymphocyte or macrophage function are prone to develop CNS infections caused by intracellular pathogens. • The most common intracellular pathogens are the fungi, particularly Aspergillus, other bacteria (e.g., Nocardia), viruses (i.e., HSV, JC, CMV, HHV-6), and parasites (e.g., T. gondii). T-lymphocyte defects • Patients with T-lymphocyte defects presenting with meningitis generally have meningitis caused by Cryptococcus or Listeria rather than toxoplasmosis or CMV infection. • The presence of extra-CNS sites of infection also may be helpful in diagnosis. • Ex: A patient with impaired cellular immunity with mass lesions in the lungs and brain that have appeared subacutely or chronically should suggest Nocardia or Aspergillus rather than cryptococcosis or toxoplasmosis. Presentation is key clinically • Most patients with CNS infections may be grouped into those with meningeal signs, or those with mass lesions. • Most pathogens have a predictable clinical presentation that differs from that of the normal host. The Setting Settings – HIV • HIV related CNS opportunistic infections – Nervous system opportunistic infections are seen in about 20% of AIDS cases and account for over 40% of AIDS related neurological manifestations. • In HIV there is a complex interplay of immune deficits but mainly T-cell immunity is impaired – – – – – CNS cytomegalovirus (encephalitis ) CNS cryptococcal infection (usually meningistis) Toxoplamosis (usually abscess) HIV encephalitis actually involves HIV cells in CNS Less common : progressive multifocal leukoencephalopathy, herpes simplex and zoster infections and tuberculosis. HIV and Cryptococcus • • • • • Cryptococcal meningitis is the most frequent fungal disease; a high degree of clinical suspicion is required in patients with fever, malaise, headache or seizures. CSF cultures are nearly always positive Both serum and CSF cryptococcal antigen tests are highly sensitive and specific. Treatment with amphotericin B and flucytosine is successful in at least 70% of first episodes but side-effects are common. Without maintenance therapy 50% of patients relapse; fluconazole is recommended. HIV and CNS toxoplamosis • Cerebral toxoplasmosis can present with focal cerebral or spinal cord signs but also as a diffuse encephalopathy • Negative T. gondii serology is unusual but positive serum titers are usually not helpful. • Treatment with sulfadiazine, pyrimethamine and folinic acid achieves good results in 90% of the first episodes, (side-effects common). • Appearances on CT scan or MRI may take several weeks to improve. Neurosyphilis and HIV • HIV disease appears to increase the likelihood of neurosyphilis, and the risk of relapse after conventional penicillin doses • At least 3-4 weeks of appropriate therapy are recommended. Aspergillus • Aspergillus infections present either as mass lesions (e.g., brain abscess), or as cerebral infarcts, but rarely as meningitis. Transplants • Infection of the CNS occurs in 5% to 10% of transplant patients and most often manifests as brain abscess, encephalitis, or meningitis. • Aspergillus fumigatus, Listeria monocytogenes, and Cryptococcus neoformans are the most common causes of CNS infections in post-transplant patients. Transplantation • • • • Susceptibility to CNS infection after transplantation changes over time. During the first month, CNS infection is most often caused by common bacterial pathogens or opportunistic pathogens present in either the transplant environment (e.g., Aspergillus species), or host (e.g., Mycobacterium tuberculosis). At 1 to 6 months, immunosuppression is at its highest, resulting in increased susceptibility to CNS infection by the herpesviruses, especially CMV and Epstein-Barr virus (EBV), fungi, and atypical bacteria. After 6 months, reduction of immunosuppression is accompanied by decreased susceptibility to CNS infection. Most cases of PML and cryptococcal meningitis occur 6 months post-transplantation. Specific pathogens – actors Viruses Cytomegalovirus - CMV • • • • Between 50% and 80% of adults in the United States are infected with CMV by 40 years of age CMV is the most common virus transmitted to fetus Approximately 1 in 150 children is born with congenital CMV Approximately 1 in 750 children is born with or develops permanent disabilities due to CMV CMV • Transmission of CMV occurs from person to person, through close contact with body fluids (urine, saliva, breast milk, blood, tears, semen, and vaginal fluids), – • • • the chance of getting CMV infection from casual contact is very small. In the United States, about 1%-4% of uninfected mothers have primary CMV infection during a pregnancy. 1/3 of women with primary CMV during pregnancy transmit to their fetus NO approved treatments for pregnant women whose fetuses might be infected with CMV. CMV • Cytomegalovirus –commonly infects neurons, glia, ependyma • Often very hard to define infection versus disease in immunocompromised hosts • CMV disease requires clinical signs and symptoms, such as fever, leukopenia, or organ involvement (including hepatitis, pneumonitis, pancreatitis, colitis, meningoencephalitis, and rarely myocarditis) • “viral load “ JC • Probable cause of most cases of progressive multifocal leukoencephalopathy • Targets myelinating oligodendrocytes • An opportunistic infection in HIV patients causing dementia like process • Diagnosed by spinal fluid PCR HH6- Human Herpes 6 • B – cell lymphotrophic virus that is the cause of roseola – and a frequent cause of febrile seizures • Reactivation occurs in immune compromised adults with HIV and lymphoma and has a possible role in multiple sclerosis and progressive multifocal leukoencephalopathy. Herpes simplex • • • • • HSV-1 infection in the immunocompromised host causes more morbidity and mortality than in the general population 62 percent of fatalities following renal transplantation were caused by viruses, with HSV contributing in 60 percent In a cohort of bone marrow transplant recipients, 82 percent of seropositive patients developed reactivation of HSV after transplantation The prevalence of HSV-1 cutaneous infections in HIV-infected patients is in the range of 5 to 20 percent . Lesions tend to be more severe than in immunocompetent hosts, with local destruction and persistent shedding of virus. Toll-like receptors are important in the innate immune response. TLRs may prevent spread of HSV from the epithelium to the brain via cranial nerves through generation of interferons. Two known mutations in TLRs predispose children to HSV encephalitis Fungi Fungal CNS infections • With the exception of Candida albicans ( normal flora of mucosa) most fungi get into the body through the airway or breaks in the skin • Invasion of the CNS with fungi can cause acute or chronic meningitis, encephalitis, abscess or granuloma, stroke, or myelopathy . • A variety of fungi lead to CNS infection Diffuse--- meningitis mainly Coccidiodomycosis Cryptococcosis Candidiasis Focal--- filamentous fungi cause granuloma or brain abscess more often than meningitis Aspergillosis Mucormycosis • Acute (sometimes called neutrophilic meningitis) has been most frequently seen in Candida meningitis • Cryptococcus neoformans typically causes the chronic lymphocytic meningitis • Coccidioides immitis causes granulomatous meningitis. Cryptococcal CNS disease • The majority of cryptococcoses begin as a primary pulmonary infection. • 5-10% of HIV + hosts develop cryptococcal meningitis as an AIDS associated disease • 40% of cases = first manifestation HIV Candida CNS disease • Candida species = normal flora of the mucous membranes and skin. • C albicans= the most frequent cause of meningitis and brain abscess among Candida species. • Less common pathogens species are C. tropicalis, C parapsilosis, C lusitaniae, C glabrata and C krusei. • Candida meningitis is more common in infants/ neonates than in older patients. CNS Candida • In newborns, candidiasis of CNS is an infection of the compromised or premature child. • Candida meningitis associated with neurosurgery • Long term antibiotics, steroids, immunosuppressive and chemotherapeutic agents, neutropenia and AIDS promote hematogenous dissemination CNS Candida • Up to 64 percent of neonates dying with invasive candidiasis have CNS involvement • More than 2/3 of these babies have positive CSF cultures at some point during their disease. Candida –scattered brain abscesses • Multiple disseminated micro-abscesses with little or no meningeal involvement have been consistently found in between 18 to 52% of patients dying with invasive candidiasis. • Very few cases of primary Candida brain abscesses have been reported in the literature. Most have been secondary to a primary source of candidiasis, including previous untreated episodes of candidemia. Aspergilllus • • • Aspergillus is ubiquitous saprophyte organism in soil, water and decaying vegetation. – a filamentous fungus Enters the body through the respiratory tract and paranasal sinuses .The invasion to CNS follows a contiguous focus infection anatomically near to the brain or by the hematogenous seeding. In addition to primary infection of lungs, hematogenous dissemination is also initiated by invasion into bloodstream via the middle ear, paranasal sinuses, eye, and mastoid or as a result of open-heart operation • Prolonged neutropenia and use of high-dose of corticosteroids are the main predisposing factors in patients with solid organ transplant and cancers • Abscesses of brain are common in disseminated aspergillosis Aspergillus • • • The genus Aspergillus includes over 185 species. Around 20 species have so far been reported as causative agents of opportunistic infections in man. Aspergillus niger is responsible for the black color you see in weathered wood and is a common fungus found in splinters. Immune suppression is the major factor predisposing to development of opportunistic infections with Aspergillus • It is the second most commonly recovered fungus in opportunistic mycoses following Candida • Almost any organ or system in the human body may be involved including cerebral aspergillosis and meningitis. Aspergillus…..we make our own food Disseminated infections can be seen in immunocompromised hosts. Aspergillus produces aggressive infection by invading a cerebral vessel producing hemorrhage and thrombosis. Zygomycetes • • • • CNS zygomycosis is a fungal infection caused by class Zygomycetes such as the Genera Rhizopus, Rhizomucor, Absidia, Mucor, Cunninghamella opportunistic fungal infection distribution of its different clinical types is more according to predisposing factors than on gender, race, age or geography. Zygomycetes thrive in a highly acid condition that has rich carbohydrate. – – diabetic ketoacidosis patient @ risk of defective phagocyte function and offers an environment for quick invasion Zygomycetes proliferate in neutropenic patients whose serum iron concentration is increased by deferoxamine Mucormycosis- (a Zygomycete) • • • • • • Mucor spp. - filamentous fungi found in soil, plants, decaying fruits and vegetables. As well as being ubiquitous in nature and a common laboratory contaminant, Mucor spp. may cause infections in man, frogs, amphibians, cattle, and swine. Mucormycosis is associated with the acidotic diabetics, malnourished children, and severely burned patients. Also seen in patients with leukemia, lymphoma, AIDS, and those on immunosuppressive therapy with corticosteroids. The infection typically involves the rhino-facial-cranial area, lungs, gastrointestinal tract, skin, or less commonly other organ systems. The fungi show a predilection for vessel (arterial) invasion resulting in embolization and necrosis of surrounding tissue. The organism creates its own nutritional source. Rhinocerebral disease in acidotic patients usually results in death, often within a few days. Rhinocerebral Mucormycosis Dimorphic fungi • • Among dimorphic fungi C. immitis and Histoplasma capulatum are the frequent organisms causing infections of the CNS. Coccidiodes immitis – A frequent cause of meningitis – geographically limited to Southwest United States and South America countries . – Coccidial meningitis happens in 3050% of patients with disseminated infection. – Can occur in an immunocomponent human. – Patients with HIV positive, solid organ transplant, treated by steroids and pregnancy are at a high risk of dissemination Coccidiomycosis • • • Endemic in southwest United States most cases are sub-clinical. Most common in males and agricultural workers. It is primarily a disease of the healthy and disseminates from a primary pulmonary site with about 30 - 50% risk of CNS involvement. Focal symptoms are uncommon, chronic meningitis is common. CNS Coccidiomycosis • • Although coccidioidomycosis usually occurs in otherwise healthy immunocompetent hosts, it may also develop in immunocompromised patients( AIDS and organ transplant recipients). This is especially true when coccidioidomycosis is in the CNS. Histoplamosis • • Histoplasmosis caused by H. capsulatum is endemic in the United States, South America, Southeast Asia and Africa . At risk populations – AIDS patients CNS – patients who have solid organ transplantation – patients treated with steroids. Histoplasmosis • Inhalation route – found in soil contaminated with bird droppings • Common in HIV-AIDS • Initial phase is flulike illness with fever and myalgias and cough • Chronic phase with dissemination • Mediastinitis commonly fatal and refractory to treatment Bob Dylan – ‘The answer is blowin in the wind” Histoplasmosis • Central nervous system involvement occurs in 5 to 20 percent of cases of disseminated histoplasmosis and is more common in those with underlying immunosuppressive disorders • Clinical presentations include (in immunocompromised): – – – – – Meningitis plus other symptoms of disseminated histoplasmosis Isolated chronic meningitis Focal brain lesions Encephalitis Localized involvement of the spinal cord Cryptococcus neoformans • • • • • Cryptococcus neoformans is the causative agent of Cryptococcosis. Given the neurotropic nature of the fungus, the most common clinical form of cryptococcosis is meningoencephalitis. The most commonly encountered predisposing factor =AIDS Less common, organ transplant recipients or cancer patients receiving chemotherapeutics or long-term corticosteroid treatment. Cryptococcosis may also involve the skin, lungs, prostate gland, urinary tract, eyes, myocardium, bones, and joints The course of the infection is usually subacute or chronic. Cryptococcus • Globose to ovoid yeast cells that have a capsule • Do not produce well-developed pseudohyphae nor true hyphae. • Candida forms well-developed pseudohyphae. Parasites Toxoplasmosis Arthur Ashe • • Toxoplasmosis is the leading cause of focal central nervous system (CNS) disease in AIDS. CNS toxoplasmosis in HIV-infected patients is usually a complication of the late phase of the disease. Typically, lesions are found in the brain and their effects dominate the clinical presentation. Rarely, intraspinal lesions need to be considered in the differential diagnosis of myelopathy Toxoplasmosis • CNS toxoplasmosis results from infection by the intracellular parasite Toxoplasma gondii. • Almost always due to reactivation of old CNS lesions or to hematogenous spread of a previously acquired infection. • Rarely, it results from primary infection Toxoplasmosis • • • CNS toxoplasmosis begins with constitutional symptoms and headache. Later, confusion and drowsiness, seizures, focal weakness, and language disturbance develop. Without treatment, patients progress to coma in days to weeks. On physical examination, personality and mental status changes may be observed. Seizures, hemiparesis, hemianopsia, aphasia, ataxia, and cranial nerve palsies may be evident. Occasionally, symptoms and signs of a radiculomyelopathy predominate. Toxoplasmosis • • • • • Cerebral toxoplasmosis is typically a disease of the immunocompromised. There is an acute onset of focal neurological deficit over a few days. The deficits are usually hemispherical (hemiparesis, apraxia, visual field defect etc) but may less commonly present with brainstem or cerebellar signs. There is commonly clouding of consciousness with fever and constitutional symptoms. Imaging shows well defined, ring enhancing, lesions with surrounding edema. Lesions are most commonly found in the cortex and grey matter of the diencephalon. Toxoplasmosis Naegleria Pathogen: Naegleria fowleri Route of entry: Contaminated water, through cribriform plate Age: Children, young adults The Case A 9-year-old boy was admitted to a hospital in Este, a small town in the Veneto region (northern Italy), with a 1-day history of fever and persistent headache on the right side. The child swam and played in a small swimming hole associated with the Po River in northern Italy 10 days before the onset of symptoms. At the time, the region was experiencing an unusually hot summer. Naegleria • A retrograde neuronal (ie, olfactory and peripheral nerves) pathway Naegleria fowleri • Infection believed to be introduced through nasal cavity and olfactory neuroepithelium • Symptoms include headache, lethargy, disorientation, coma • Usually summer or fall (when we get in water) • Rapid clinical course, death in 2-7 days after onset of symptoms • Trophozoites can be detected in spinal fluid, but diagnosis is usually at autopsy….PCR • 4 known survivors treated with Amphotericin B Acanthamoeba • Pathogen: Acanthamoeba castellanii • • Route of entry: Probably sinus, skin lesion, eye Anatomic Sites: Anywhere in the brain can be involved but the cerebellum, brain stem, thalamus and anterior parts of the cerebrum are most severely affected; the spinal cord is usually spared. Acanthamoeba • • • • • • • May or may not have history of swimming or exposure to contaminated water; Presents as a subacute or chronic meningoencephalitis; Symptoms include headache, fever, mental abnormalities, hemiparesis and seizures; Patients may be immunocompromised or have HIV infection, or having some chronic disease such as diabetes. Trophozoites: 15-45 mm in diameter, nucleus with a dense central nucleolus, cytoplasm contains granules and vacuoles Trophozoites be found in the vessel wall and in areas free of inflammatory cell infiltration. Cystic forms: in the tissue (15-20 mm in diameter) characterized by wrinkled double wall around a stellate endocyst Bacteria Nocardia • Nocardia asteroides is a filamentous aerobic gram positive bacterium that generally enters the body through the respiratory system. • Initial symptoms are that of pulmonary infection with cough, fever and sputum production • Dissemination involving the organ with brain abscess and subcutaneous nodules being the most frequent. This is seen exclusively in immunocompromised patients • Delay of diagnosis = poor outcome. “Hole in the lung/ hole in the brain “ Not really opportunists per se Echinococcus Echinococcus • • • • • • • Echinococcosis in humans is also called hydatid cyst disease Hydatid disease caused by Echinococcus granulosis is primarily found in Alaska, California, and the South-West E. multilocularis more common in the North-Central Dogs and wolves are definitive hosts of E. granulosis Dogs and foxes are definitive hosts of E. multilocularis. Dogs become infected with E. granulosis by ingesting sheep or goat intermediate host viscera containing infective hydatid cysts; E. multilocularis involves rodent intermediate hosts. Transmission to humans takes place by accidental ingestion of ova of Echinococcus shed in feces of infected dogs. Echinococcus • • • • • Humans become infected with E. granulosis when they accidentally ingest eggs in contaminated foods, on vegetables or on blades of grass. Although uncommon, this disease is potentially fatal and is on the increase. Cerebral echinococcosis should be kept in mind in the differential diagnosis of cerebral cystic lesions, especially in the endemic areas, where hydatid disease is a common problem. Hydatid cysts may mimic brain tumors so a preoperative diagnosis is important especially in endemic areas. Intracranial hydatid cysts should always be surgically removed without rupture. Proper preoperative diagnosis is critical for the successful outcome of surgery. The outcome remains excellent for unruptured cysts. Malaria as an opportunist (Mal =bad / Aria= air) • HIV increases the risk of malaria infection and the development of clinical malaria. Conversely, malaria increases HIV replication. • Pregnant women transiently lose some of their acquired immunity due to the relative immunosuppression of pregnancy Malaria • • • • Cerebral malaria (CM) involves the clinical manifestations of Plasmodium falciparum malaria that induce changes in mental status and coma. It is an acute, widespread disease of the brain which is accompanied by fever. The mortality ratio is between 25-50%. Untreated, CM is fatal in 24-72 hours. The histopathological hallmark of encephalopathy is the sequestration of cerebral capillaries and venules with parasitized red blood cells (PRBCs) and non-PRBCs (NPRBCs). Ring-like lesions in the brain are major characteristics. Risk factors include being a child under 10 years of age and living in malaria-endemic area. Malaria • • In terminal cases blocked capillaries in the brain cause it to become swollen and congested. Brains of persons who die of cerebral malaria show congestion and thrombosis of small blood vessels in the white matter, which are rimmed with edema and hemorrhage (“ring hemorrhages”). Malaria • Malarial pigment can also be seen in the capillaries; proteinaceous material may be seen around the involved vessels • There is necrosis of the perivascular white matter, and focal loss of myelin staining, also accumulation of reactive microglia and astrocytes in the vicinity. Dengue virus • • • • One-third of the world’s population living in areas at risk for transmission, dengue infection is a leading cause of illness and death in the tropics and subtropics with 100 million people are infected yearly. Dengue is caused by any one of four related viruses transmitted by mosquitoes (Aedes aegypti). There are no vaccines to prevent infection with dengue virus (DENV). Symptoms of dengue fever include fever, retro-orbital pain, joint pain and muscle pain – break bone fever. The initial illness is much milder than repeat infections with the virus Dengue • • • Encephalopathy is the most common neurological manifestation. It may result from hypotension, cerebral edema, microvascular and frank hemorrhage, hyponatremia, and fulminant hepatic failure which may be part of Reye‘s Syndrome. These metabolic factors are held responsible for neurological manifestations when the virus or its serological evidence cannot be found in the CSF. Animal studies have shown a virus mediated breakdown of the blood-brain barrier. Measles – SSPE • • • • The family of Paramyxoviridae contains viruses that induce a wide range of distinct clinical illnesses in humans. These include measles virus, which in rare instances is followed by subacute sclerosing panencephalitis (SSPE). SSPE is a late complication central nervous system infection of measles virus occurring 5 to 15 years after infection. It occurs more often in males who developed measles early in life and causes a CNS degenerative disease. High levels of antibody to measles virus are found in Serum and CSF and it is apparent that intrathecal immunoglobulin is synthesized in this disorder. Syphilis - Leues • Sexually-transmitted disease caused by Treponema pallidum, a spirochetal organism • Often called the great imitator Syphilis - Leues • • • • Primary syphilis: (Treponema pallidum), - 10 to 90 days. The first symptom of primary syphilis is often a single, small, round, painless sore, called a chancre. Secondary syphilis: symptoms can begin 2 to 10 weeks after the chancre sore appears. The most common symptom is a rash on the palms of the hands and the bottoms of the feet. The symptoms appear to resolve with or without treatment. Latent syphilis: This stage can start from 2 years to over 30 years after the initial infection. In late latent syphilis, the infection is quiet and the risk of infecting a sexual partner is low or absent. Tertiary syphilis: In this stage of syphilis, the bacteria can damage almost any part of the body, but most commonly affects the Heart, Eyes, Brain, Nervous system, Bones and joints, liver Syphilis - Leues • • • • Late neurosyphilis (brain or spinal cord damage) is one of the most severe signs of this stage. An example of neurosyphilis is a disease called tabes dorsalis. It occurs in persons with untreated syphilis many years after they are first infected. Neurosyphilis is an infection of the brain or spinal cord. It occurs in persons with untreated syphilis many years after they are first infected. Neurosyphilis may be asymptomatic, with findings only on examination of cerebrospinal fluid. The usual findings on exam of CSF are presence of white blood cells, elevated protein, and a reactive serologic test for syphilis (the VDRL is generally accepted as the standard test for CSF). It is vital to understand that, in the presence of HIV infection, neurosyphilis in any of its manifestations may become apparent within weeks to months of primary syphilitic infection Syphilis - Leues • • • • • • • • • • Abnormal walk (gait) Blindness Confusion Dementia Depression Headache Incontinence Inability to walk Irritability Loss of muscle function • • • • • • • • • Mental decline Paralysis Poor concentration Seizures Stiff neck Tremors Visual disturbances Weakness, numbness of lower extremities Note: There may be no symptoms Syphilis - Leues • Penicillin is used to treat neurosyphilis by injection IV daily for 10 - 14 days or with probenecid by mouth 4 times a day, combined with daily IM -both for 10 - 14 days. • Follow-up blood tests and lumbar punctures for CSF fluid analysis at 3, 6, 12, and 24 to establish cure. Lyme disease • • • Lyme disease is caused by the bacterium Borrelia burgdorferi and is transmitted to humans by the bite of infected blacklegged ticks. Typical symptoms include fever, headache, fatigue, and a characteristic skin rash called erythema migrans. If left untreated, infection can spread to joints, the heart, and the nervous system. The organism is a spirochetal organism. Lyme disease – 3 stages • Stage I – early localized infection characterized by a bull’s-eye rash called erythema chronicum migrans Lyme disease – 3 stages • Stage II – early disseminated infection with 15% having neurologic symptoms including Bell’s palsy. Patient may experience radiculopathies, meningitis or mild encephalitis. Some cases of neuroborreliosis have only altered mental status and the diagnosis may therefore be elusive. Lyme disease • Stage III – late persistent infection which is characterized by: – Polyneuropathy with abnormal sensation in hands and feet • Mostly sensory – Lyme encephalopathy with memory and cognitive dysfunction – Chronic encephalomyelitis cognitive impairment, weakness in the legs, awkward gait, facial palsy, bladder problems, vertigo and occasionally psychiatric disorders. So be careful • • • • • • • • • • • • • Don’t travel to Southwest …coccidiomycosis Don’t eat fuzzy strawberries. … zygomycetes Don’t rob King Tut –the curse is Aspergillus Don’t eat undercooked mutton….Echinococcus Don’t get dengue a second time… Stay out of the Mississippi River Valley …Histo Keep your contacts clean….. Acanthamoeba Don’t eat poorly cooked pork / lamb/ beef…. Toxoplamosis Don’t assassinate the cat…. Toxo Only deal with potty trained birds…. Cryptococcus Stay out of the fountain…. Naegleria fowleri Don’t ask my daughter for answers…… I gave her all the wrong answers Stay away from heart shaped tubs