Made by DATEXIS (Data Science and Text-based Information Systems) at Beuth University of Applied Sciences Berlin
Deep Learning Technology: Sebastian Arnold, Betty van Aken, Paul Grundmann, Felix A. Gers and Alexander Löser. Learning Contextualized Document Representations for Healthcare Answer Retrieval. The Web Conference 2020 (WWW'20)
Funded by The Federal Ministry for Economic Affairs and Energy; Grant: 01MD19013D, Smart-MD Project, Digital Technologies
In adults, the most common symptom of meningitis is a severe headache, occurring in almost 90% of cases of bacterial meningitis, followed by nuchal rigidity (the inability to flex the neck forward passively due to increased neck muscle tone and stiffness). The classic triad of diagnostic signs consists of nuchal rigidity, sudden high fever, and altered mental status; however, all three features are present in only 44–46% of bacterial meningitis cases. If none of the three signs are present, acute meningitis is extremely unlikely. Other signs commonly associated with meningitis include photophobia (intolerance to bright light) and phonophobia (intolerance to loud noises). Small children often do not exhibit the aforementioned symptoms, and may only be irritable and look unwell. The fontanelle (the soft spot on the top of a baby's head) can bulge in infants aged up to 6 months. Other features that distinguish meningitis from less severe illnesses in young children are leg pain, cold extremities, and an abnormal skin color.
Nuchal rigidity occurs in 70% of bacterial meningitis in adults. Other signs include the presence of positive Kernig's sign or Brudziński sign. Kernig's sign is assessed with the person lying supine, with the hip and knee flexed to 90 degrees. In a person with a positive Kernig's sign, pain limits passive extension of the knee. A positive Brudzinski's sign occurs when flexion of the neck causes involuntary flexion of the knee and hip. Although Kernig's sign and Brudzinski's sign are both commonly used to screen for meningitis, the sensitivity of these tests is limited. They do, however, have very good specificity for meningitis: the signs rarely occur in other diseases. Another test, known as the "jolt accentuation maneuver" helps determine whether meningitis is present in those reporting fever and headache. A person is asked to rapidly rotate the head horizontally; if this does not make the headache worse, meningitis is unlikely.
Other problems can produce symptoms similar to those above, but from non-meningitic causes. This is called meningism or pseudomeningitis.
Meningitis caused by the bacterium "Neisseria meningitidis" (known as "meningococcal meningitis") can be differentiated from meningitis with other causes by a rapidly spreading petechial rash, which may precede other symptoms. The rash consists of numerous small, irregular purple or red spots ("petechiae") on the trunk, lower extremities, mucous membranes, conjuctiva, and (occasionally) the palms of the hands or soles of the feet. The rash is typically non-blanching; the redness does not disappear when pressed with a finger or a glass tumbler. Although this rash is not necessarily present in meningococcal meningitis, it is relatively specific for the disease; it does, however, occasionally occur in meningitis due to other bacteria. Other clues on the cause of meningitis may be the skin signs of hand, foot and mouth disease and genital herpes, both of which are associated with various forms of viral meningitis.
Additional problems may occur in the early stage of the illness. These may require specific treatment, and sometimes indicate severe illness or worse prognosis. The infection may trigger sepsis, a systemic inflammatory response syndrome of falling blood pressure, fast heart rate, high or abnormally low temperature, and rapid breathing. Very low blood pressure may occur at an early stage, especially but not exclusively in meningococcal meningitis; this may lead to insufficient blood supply to other organs. Disseminated intravascular coagulation, the excessive activation of blood clotting, may obstruct blood flow to organs and paradoxically increase the bleeding risk. Gangrene of limbs can occur in meningococcal disease. Severe meningococcal and pneumococcal infections may result in hemorrhaging of the adrenal glands, leading to Waterhouse-Friderichsen syndrome, which is often fatal.
The brain tissue may swell, pressure inside the skull may increase and the swollen brain may herniate through the skull base. This may be noticed by a decreasing level of consciousness, loss of the pupillary light reflex, and abnormal posturing. The inflammation of the brain tissue may also obstruct the normal flow of CSF around the brain (hydrocephalus). Seizures may occur for various reasons; in children, seizures are common in the early stages of meningitis (in 30% of cases) and do not necessarily indicate an underlying cause. Seizures may result from increased pressure and from areas of inflammation in the brain tissue. Focal seizures (seizures that involve one limb or part of the body), persistent seizures, late-onset seizures and those that are difficult to control with medication indicate a poorer long-term outcome.
Inflammation of the meninges may lead to abnormalities of the cranial nerves, a group of nerves arising from the brain stem that supply the head and neck area and which control, among other functions, eye movement, facial muscles, and hearing. Visual symptoms and hearing loss may persist after an episode of meningitis. Inflammation of the brain (encephalitis) or its blood vessels (cerebral vasculitis), as well as the formation of blood clots in the veins (cerebral venous thrombosis), may all lead to weakness, loss of sensation, or abnormal movement or function of the part of the body supplied by the affected area of the brain.
The patient with meningococcal meningitis typically presents with high fever, nuchal rigidity (stiff neck), Kernig's sign, severe headache, vomiting, purpura, photophobia, and sometimes chills, altered mental status, or seizures. Diarrhea or respiratory symptoms are less common. Petechiae are often also present, but do not always occur, so their absence should not be used against the diagnosis of meningococcal disease. Anyone with symptoms of meningococcal meningitis should receive intravenous antibiotics before the results of lumbar puncture, as delay in treatment worsens the prognosis.
Possible symptoms of "Haemophilus" meningitis include:
- Nausea or vomiting
- Fever
- Headache
- Sensitivity to light
- Seizures
- Anorexia
- change in mental status, such as irritability
- stiff neck
Symptoms of meningococcemia are, at least initially, similar to those of influenza. Typically, the first symptoms include fever, nausea, myalgia, headache, arthralgia, chills, diarrhea, stiff neck, and malaise. Later symptoms include septic shock, purpura, hypotension, cyanosis, petechiae, seizures, anxiety, and multiple organ dysfunction syndrome. Acute respiratory distress syndrome and altered mental status may also occur. The petichial rash appear with the 'star-like' shape. Meningococcal sepsis has a greater mortality rate than meningococcal meningitis, but the risk of neurologic sequelae is much lower.
The following is a list of common signs and symptoms found with neonatal meningitis.
- Fever
- poor appetite
- anterior fontanelle bulging
- seizure
- jitteriness
- dyspnea
- irritability
- anorexia
- vomiting
- diarrhea
- abdominal distention (increase in abdominal size)
- neck rigidity
- cyanosis
- jaundice
- and sunset eyes (downward gaze of the eyes)
- abnormal body temperature (hypo-or hyperthermia)
- change of activity (lethargy or irritability)
Unfortunately these symptoms are unspecific and may point to many different conditions.
Fever and headache are the cardinal features, confusion is a late feature and coma bears a poor prognosis. Meningism is absent in a fifth of patients with TB meningitis. Patients may also have focal neurological deficits.
"Haemophilus" meningitis is a form of bacterial meningitis caused by the "Haemophilus influenzae" bacteria. It is usually (but not always) associated with "Haemophilus influenzae" type b. Meningitis involves the inflammation of the protective membranes that cover the brain and spinal cord. "Haemophilus" meningitis is characterized by symptoms including fever, nausea, sensitivity to light, headaches, stiff neck, anorexia, and seizures. "Haemophilus" meningitis can be deadly, but antibiotics are effective in treating the infection, especially when cases are caught early enough that the inflammation has not done a great deal of damage. Before the introduction of the Hib vaccine in 1985, Haemophilus meningitis was the leading cause of bacterial meningitis in children under the age of five. However, since the creation of the Hib vaccine, only two in every 100,000 children contract this type of meningitis. Five to ten percent of cases can be fatal, although the average mortality rate in developing nations is seventeen percent, mostly due to lack of access to vaccination as well as lack of access to medical care needed to combat the meningitis.
Neonatal meningitis is a serious medical condition in infants. Meningitis is an inflammation of the meninges (the protective membranes of the central nervous system (CNS)) and is more common in the neonatal period (infants less than 44 days old) than any other time in life and is an important cause of morbidity and mortality globally. Mortality is roughly half in developing countries and ranges from 8%-12.5% in developed countries.
Symptoms seen with neonatal meningitis are often unspecific that may point to several conditions, such as sepsis (whole body inflammation). These can include fever, irritability, and dyspnea. The only method to determine if meningitis is the cause of these symptoms is lumbar puncture (LP; an examination of the cerebrospinal fluid).
The most common causes of neonatal meningitis is bacterial infection of the blood, known as bacteremia (specifically Group B "Streptococci" (GBS; "Streptococcus agalactiae"), "Escherichia coli", and "Listeria monocytogenes"). Although there is a low mortality rate in developed countries, there is a 50% prevalence rate of neurodevelopmental disabilities in "E. coli" and GBS meningitis, while having a 79% prevalence for non-"E. coli" Gram-negative caused meningitis. Delayed treatment of neonatal meningitis may cause include cerebral palsy, blindness, deafness, and learning deficiencies.
Mycobacterium tuberculosis of the meninges is the cardinal feature and the inflammation is concentrated towards the base of the brain. When the inflammation is in the brain stem subarachnoid area, cranial nerve roots may be affected. The symptoms will mimic those of space-occupying lesions.
Blood-borne spread certainly occurs, presumably by crossing the blood–brain barrier; but a proportion of patients may get TB meningitis from rupture of a cortical focus in the brain; an even smaller proportion get it from rupture of a bony focus in the spine.
Causative organisms include protozoans, viral and bacterial pathogens.
Specific types include:
Viral meningitis characteristically presents with fever, headache and neck stiffness. Fever is the result of cytokines released that affect the thermoregulatory neurons of the hypothalamus. Cytokines and increased intracranial pressure stimulate nociceptors in the brain that lead to headaches. Neck stiffness is the result of inflamed meninges stretching due to flexion of the spine. In contrast to bacterial meningitis, symptoms are often less severe and do not progress as quickly. Nausea, vomiting and photophobia (light sensitivity) also commonly occur, as do general signs of a viral infection, such as muscle aches and malaise. Increased cranial pressure from viral meningitis stimulates the area postrema, which causes nausea and vomiting. Photophobia is due to meningeal irritation. In severe cases, people may experience concomitant encephalitis (meningoencephalitis), which is suggested by symptoms such as altered mental status, seizures or focal neurologic deficits.
Babies with viral meningitis may only appear irritable, sleepy or have trouble eating. In severe cases, people may experience concomitant encephalitis (meningoencephalitis), which is suggested by symptoms such as altered mental status, seizures or focal neurologic deficits. The pediatric population may show some additional signs and symptoms that include jaundice and bulging fontanelles.
Pneumococcal infection is an infection caused by the bacterium "Streptococcus pneumoniae". "S. pneumoniae" is a common member of the bacterial flora colonizing the nose and throat of 5–10% of healthy adults and 20–40% of healthy children. However, it is also the cause of significant disease being a leading cause of pneumonia, bacterial meningitis, and sepsis. The World Health Organization estimate that in 2005 pneumococcal infections were responsible for the death of 1.6 million children worldwide.
Ameobic pathogens exist as free-living protozoans. Nevertheless, these pathogens cause rare and uncommon CNS infections. N. fowleri produces primary amebic meningoencephalitis (PAM). The symptoms of PAM are indistinguishable from acute bacterial meningitis. Other amebae cause granulomatous amebic encephalitis (GAE), which is a more subacute and can even a non-symptomatic chronic infection. Ameobic meningoencephalitis can mimic a brain abscess, aseptic or chronic meningitis, or CNS malignancy.
Symptoms of fungal meningitis are generally similar to those of other types of meningitis, and include: a fever, stiff neck, severe headache, photophobia (sensitivity to light), nausea and vomiting, and altered mental status (drowsiness or confusion).
Aseptic meningitis, or sterile meningitis, is a condition in which the layers lining the brain, the meninges, become inflamed and a pyogenic bacterial source is not to blame. Meningitis is diagnosed on a history of characteristic symptoms and certain examination findings (e.g., Kernig's sign). Investigations should show an increase in the number of leukocytes present in the cerebrospinal fluid (CSF) obtained via lumbar puncture (normally being fewer than five visible leukocytes per microscopic high-power field).
The term "aseptic" is frequently a misnomer, implying a lack of infection. On the contrary, many cases of aseptic meningitis represent infection with viruses or mycobacteria that cannot be detected with routine methods. While the advent of polymerase chain reaction has increased the ability of clinicians to detect viruses such as enterovirus, cytomegalovirus, and herpes virus in the CSF, many viruses can still escape detection. Additionally, mycobacteria frequently require special stains and culture methods that make their detection difficult. When CSF findings are consistent with meningitis, and microbiologic testing is unrevealing, clinicians typically assign the diagnosis of aseptic meningitis—making it a relative diagnosis of exclusion.
Aseptic meningitis can result from non-infectious causes as well. it can be a relatively infrequent side effect of medications, or be a result of an autoimmune disease. There is no formal classification system of aseptic meningitis except to state the underlying cause, if known. The absence of bacteria found in the spinal fluid upon spinal tap, either through microscopic examination or by culture, usually differentiates aseptic meningitis from its pyogenic counterpart.
"Aseptic meningitis", like non-gonococcal urethritis, non-Hodgkin lymphoma and atypical pneumonia, merely states what the condition is not, rather than what it is. Terms such as viral meningitis, bacterial meningitis, fungal meningitis, neoplastic meningitis and drug-induced aseptic meningitis can provide more information about the condition, and without using one of these more specific terms, it is difficult to describe treatment options or prognosis.
"S. pneumoniae" is responsible for 15–50% of all episodes of community acquired pneumonia, 30–50% of all cases of acute otitis media, and a significant proportion of bloodstream infections and bacterial meningitis.
As estimated by WHO in 2005 it killed about 1.6 million children every year worldwide with 0.7–1 million of them being under the age of five. The majority of these deaths were in developing countries.
Viral meningitis, also known as aseptic meningitis, is a type of meningitis due to a viral infection. It results in inflammation of the meninges (the membranes covering the brain and spinal cord). Symptoms commonly include headache, fever, sensitivity to light, and neck stiffness.
Viruses are the most common cause of aseptic meningitis. Most cases of viral meningitis are caused by enteroviruses (common stomach viruses). However, other viruses can also cause viral meningitis. For instance, West Nile virus, mumps, measles, herpes simplex types I and II, varicella, and lymphocytic choriomeningitis (LCM) virus. Based on clinical symptoms, viral meningitis cannot be reliably differentiated from bacterial meningitis, although viral meningitis typically follows a more benign clinical course. Viral meningitis has no evidence of bacteria present in cerebral spinal fluid (CSF). Therefore, lumbar puncture with CSF analysis is often needed to identify the disease.
In most causes there is no specific treatment, with efforts generally aimed at relieving symptoms (headache, fever, or nausea). A few viral causes, such as HSV, have specific treatments.
In the United States viral meningitis is the cause of greater than half of all cases of meningitis. From 1988–1999, about 36,000 cases occurred a year. While the disease can occur in both children and adults it is more common in children.
Bacillary dysentery is a type of dysentery, and is a severe form of shigellosis.
Bacillary dysentery is associated with species of bacteria from the Enterobacteriaceae family. The term is usually restricted to "Shigella" infections.
Shigellosis is caused by one of several types of "Shigella" bacteria. Three species are associated with bacillary dysentery: "Shigella sonnei, Shigella flexneri" and "Shigella dysenteriae". A study in China indicated that "Shigella flexneri" 2a was the most common serotype.
Salmonellosis caused by "Salmonella enterica" (serovar "Typhimurium") has also been described as a cause of bacillary dysentery, though this definition is less common. It is sometimes listed as an explicit differential diagnosis of bacillary dysentery, as opposed to a cause.
Bacillary dysentery should not be confused with diarrhea caused by other bacterial infections. One characteristic of bacillary dysentery is blood in stool, which is the result of invasion of the mucosa by the pathogen.
Bacteremia is the presence of bacteria in the bloodstream that are alive and capable of reproducing. It is a type of bloodstream infection. Bacteremia is defined as either a primary or secondary process. In primary bacteremia, bacteria have been directly introduced into the bloodstream. Injection drug use may lead to primary bacteremia. In the hospital setting, use of blood vessel catheters contaminated with bacteria may also lead to primary bacteremia. Secondary bacteremia occurs when bacteria have entered the body at another site, such as the cuts in the skin, or the mucous membranes of the lungs (respiratory tract), mouth or intestines (gastrointestinal tract), bladder (urinary tract), or genitals. Bacteria that have infected the body at these sites may then spread into the lymphatic system and gain access to the bloodstream, where further spread can occur.
Bacteremia may also be defined by the timing of bacteria presence in the bloodstream: transient, intermittent, or persistent. In transient bacteremia, bacteria are present in the bloodstream for minutes to a few hours before being cleared from the body, and the result is typically harmless in healthy people. This can occur after manipulation of parts of the body normally colonized by bacteria, such as the mucosal surfaces of the mouth during teeth brushing, flossing, or dental procedures, or instrumentation of the bladder or colon. Intermittent bacteremia is characterized by periodic seeding of the same bacteria into the bloodstream by an existing infection elsewhere in the body, such as an abscess, pneumonia, or bone infection, followed by clearing of that bacteria from the bloodstream. This cycle will often repeat until the existing infection is successfully treated. Persistent bacteremia is characterized by the continuous presence of bacteria in the bloodstream. It is usually the result of an infected heart valve, a central line-associated bloodstream infection (CLABSI), an infected blood clot (suppurative thrombophlebitis), or an infected blood vessel graft. Persistent bacteremia can also occur as part of the infection process of typhoid fever, brucellosis, and bacterial meningitis. Left untreated, conditions causing persistent bacteremia can be potentially fatal.
Bacteremia is clinically distinct from sepsis, which is a condition where the blood stream infection is associated with an inflammatory response from the body, often causing abnormalities in body temperature, heart rate, breathing rate, blood pressure, and white blood cell count.
Fungal meningitis may be caused by the following (and also other) types of fungi:
- "Candida" - "C. albicans" is the most common "Candida" species causing CNS infection.
- "Coccidioides" - it is endemic to southwestern United States and Mexico. A third of patients presenting with disseminated coccidioidomycosis have developed meningitis.
- "Histoplasma" - occurs in bird and bat droppings and is endemic in parts of the United States, South, and Central America. CNS involvement occurs in 10-20% of disseminated histoplasmosis cases.
- "Blastomyces" - occurs in soil rich in decaying organic matter in the Midwest United States. Meningitis is an unusual manifestation of blastomycosis and can be very difficult to diagnose.
- "Cryptococcus" (Cryptococcal meningitis) - it is thought to be acquired through inhalation of soil contaminated with bird droppings. "C. neoformans" is the most common pathogen to cause fungal meningitis.
- "Aspergillus" - "Aspergillus" infections account for 5% of CNS fungal infections.
Bacteremia (also bacteraemia) is the presence of bacteria in the blood. Blood is normally a sterile environment, so the detection of bacteria in the blood (most commonly accomplished by blood cultures) is always abnormal. It is distinct from sepsis, which is the host response to the bacteria.
Bacteria can enter the bloodstream as a severe complication of infections (like pneumonia or meningitis), during surgery (especially when involving mucous membranes such as the gastrointestinal tract), or due to catheters and other foreign bodies entering the arteries or veins (including during intravenous drug abuse). Transient bacteremia can result after dental procedures or brushing of teeth.
Bacteremia can have several important health consequences. The immune response to the bacteria can cause sepsis and septic shock, which has a high mortality rate. Bacteria can also spread via the blood to other parts of the body (which is called hematogenous spread), causing infections away from the original site of infection, such as endocarditis or osteomyelitis. Treatment for bacteremia is with antibiotics, and prevention with antibiotic prophylaxis can be given in high risk situations.
Transmission is fecal-oral and is remarkable for the small number of organisms that may cause disease (10 ingested organisms cause illness in 10% of volunteers, and 500 organisms cause disease in 50% of volunteers). "Shigella" bacteria invade the intestinal mucosal cells but do not usually go beyond the lamina propria. Dysentery is caused when the bacteria escape the epithelial cell phagolysosome, multiply within the cytoplasm, and destroy host cells. Shiga toxin causes hemorrhagic colitis and hemolytic-uremic syndrome by damaging endothelial cells in the microvasculature of the colon and the glomeruli, respectively. In addition, chronic arthritis secondary to "S. flexneri" infection, called reactive arthritis, may be caused by a bacterial antigen; the occurrence of this syndrome is strongly linked to HLA-B27 genotype, but the immunologic basis of this reaction is not understood.
The signs and symptoms of Lemierre's syndrome vary, but usually start with a sore throat, fever, and general body weakness. These are followed by extreme lethargy, spiked fevers, rigors, swollen cervical lymph nodes, and a swollen, tender or painful neck. Often there is abdominal pain, diarrhea, nausea and vomiting during this phase. These signs and symptoms usually occur several days to 2 weeks after the initial symptoms.
Symptoms of pulmonary involvement can be shortness of breath, cough and painful breathing (pleuritic chest pain). Rarely, blood is coughed up. Painful or inflamed joints can occur when the joints are involved.
Septic shock can also arise. This presents with low blood pressure, increased heart rate, decreased urine output and an increased rate of breathing. Some cases will also present with meningitis, which will typically manifest as neck stiffness, headache and sensitivity of the eyes to light.
Liver enlargement and spleen enlargement can be found, but are not always associated with liver or spleen abscesses.
Other signs and symptoms that may occur:
- Headache (unrelated to meningitis)
- Memory loss
- Muscle pain
- Jaundice
- Decreased ability to open the jaw
- Crepitations are sometimes heard over the lungs
- Pericardial friction rubs as a sign of pericarditis (rare)
- Cranial nerve paralysis and Horner's syndrome (both rare)
Lemierre's syndrome (or Lemierre's disease, also known as postanginal shock including sepsis and human necrobacillosis) refers to infectious thrombophlebitis of the internal jugular vein. It most often develops as a complication of a bacterial sore throat infection in young, otherwise healthy adults. The thrombophlebitis is a serious condition and may lead to further systemic complications such as bacteria in the blood or septic emboli.
Lemierre's syndrome occurs most often when a bacterial (e.g., "Fusobacterium necrophorum") throat infection progresses to the formation of a peritonsillar abscess. Deep in the abscess, anaerobic bacteria can flourish. When the abscess wall ruptures internally, the drainage carrying bacteria seeps through the soft tissue and infects the nearby structures. Spread of infection to the nearby internal jugular vein provides a gateway for the spread of bacteria through the bloodstream. The inflammation surrounding the vein and compression of the vein may lead to blood clot formation. Pieces of the potentially infected clot can break off and travel through the right heart into the lungs as emboli, blocking branches of the pulmonary artery that carry blood with little oxygen from the right side of the heart to the lungs.
Sepsis following a throat infection was described by Schottmuller in 1918. However, it was André Lemierre, in 1936, who published a series of 20 cases where throat infections were followed by identified anaerobic sepsis, of whom 18 patients died.