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Among the signs of subacute bacterial endocarditis are:
- Malaise
- Weakness
- Excessive sweat
- Fever
Subacute bacterial endocarditis (also called endocarditis lenta) is a type of endocarditis (more specifically, infective endocarditis). Subacute bacterial endocarditis can be considered a form of type III hypersensitivity.
Infective endocarditis may also be classified as "culture-positive" or "culture-negative". By far the most common cause of a "culture-negative" endocarditis is prior administration of antibiotics.
Sometimes microorganisms can take a longer period of time to grow in the culture media, such organisms are said to be "fastidious" because they have demanding growth requirements. Some examples include pathogens like "Aspergillus" species, "Brucella" species, "Coxiella burnetii", "Chlamydia" species, and HACEK bacteria. Due to delay in growth and identification in these cases, patients may be erroneously classified as "culture-negative" endocarditis.
Historically, infective endocarditis has been clinically divided into "acute" and "subacute" presentations (because untreated patients tended to live longer with the subacute as opposed to the acute form). This classifies both the rate of progression and severity of disease.
- "Subacute bacterial endocarditis" (SBE) is often due to streptococci of low virulence (mainly viridans streptococci) and mild to moderate illness which progresses slowly over weeks and months (>2 weeks) and has low propensity to hematogenously seed extracardiac sites.
- "Acute bacterial endocarditis" (ABE) is a fulminant illness over days to weeks (<2 weeks), and is more likely due to "Staphylococcus aureus" which has much greater virulence, or disease-producing capacity and frequently causes metastatic infection.
This classification is now discouraged, because the ascribed associations (in terms of organism and prognosis) were not strong enough to be relied upon clinically. The terms "short incubation" (meaning less than about six weeks), and "long incubation" (greater than about six weeks) are preferred.
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.
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.
The several forms of the infection are:
- Skin/subcutaneous tissue disease is a septic phlegmon that develops classically in the hand and forearm after a cat bite. Inflammatory signs are very rapid to develop; in 1 or 2 hours, edema, severe pain, and serosanguineous exudate appear. Fever, moderate or very high, can be seen, along with vomiting, headache, and diarrhea. Lymphangitis is common. Complications are possible, in the form of septic arthritis, osteitis, or evolution to chronicity.
- Sepsis is very rare, but can be as fulminant as septicaemic plague, with high fever, rigors, and vomiting, followed by shock and coagulopathy.
- Pneumonia disease is also rare and appears in patients with some chronic pulmonary pathology. It usually presents as bilateral consolidating pneumonia, sometimes very severe.
- Zoonosis, pasteurellosis can be transmitted to humans through cats.
Other locations are possible, such as septic arthritis, meningitis, and acute endocarditis, but are very rare.
Nonbacterial thrombotic endocarditis (NBTE) is most commonly found on previously undamaged valves. As opposed to infective endocarditis, the vegetations in NBTE are small, sterile, and tend to aggregate along the edges of the valve or the cusps. Also unlike infective endocarditis, NBTE does not cause an inflammation response from the body. NBTE usually occurs during a hypercoagulable state such as system-wide bacterial infection, or pregnancy, though it is also sometimes seen in patients with venous catheters. NBTE may also occur in patients with cancers, particularly mucinous adenocarcinoma where Trousseau syndrome can be encountered. Typically NBTE does not cause many problems on its own, but parts of the vegetations may break off and embolize to the heart or brain, or they may serve as a focus where bacteria can lodge, thus causing infective endocarditis.
Another form of sterile endocarditis is termed Libman–Sacks endocarditis; this form occurs more often in patients with lupus erythematosus and is thought to be due to the deposition of immune complexes. Like NBTE, Libman-Sacks endocarditis involves small vegetations, while infective endocarditis is composed of large vegetations. These immune complexes precipitate an inflammation reaction, which helps to differentiate it from NBTE. Also unlike NBTE, Libman-Sacks endocarditis does not seem to have a preferred location of deposition and may form on the undersurfaces of the valves or even on the endocardium.
Diagnosis is made with isolation of "Pasteurella multocida" in a normally sterile site (blood, pus, or cerebrospinal fluid).
Endocarditis is an inflammation of the inner layer of the heart, the endocardium. It usually involves the heart valves. Other structures that may be involved include the interventricular septum, the chordae tendineae, the mural endocardium, or the surfaces of intracardiac devices. Endocarditis is characterized by lesions, known as "vegetations", which is a mass of platelets, fibrin, microcolonies of microorganisms, and scant inflammatory cells. In the subacute form of infective endocarditis, the vegetation may also include a center of granulomatous tissue, which may fibrose or calcify.
There are several ways to classify endocarditis. The simplest classification is based on cause: either "infective" or "non-infective", depending on whether a microorganism is the source of the inflammation or not. Regardless, the diagnosis of endocarditis is based on clinical features, investigations such as an echocardiogram, and blood cultures demonstrating the presence of endocarditis-causing microorganisms. Signs and symptoms include fever, chills, sweating, malaise, weakness, anorexia, weight loss, splenomegaly, flu-like feeling, cardiac murmur, heart failure, petechia of anterior trunk, Janeway's lesions, etc.
Acute prostatitis is a serious bacterial infection of the prostate gland. This infection is a medical emergency. It should be distinguished from other forms of prostatitis such as chronic bacterial prostatitis and chronic pelvic pain syndrome (CPPS).
Men with acute prostatitis often have chills, fever, pain in the lower back, perineum, or genital area, urinary frequency and urgency often at night, burning or painful urination, body aches, and a demonstrable infection of the urinary tract, as evidenced by white blood cells and bacteria in the urine. Acute prostatitis may be a complication of prostate biopsy. Often, the prostate gland is very tender to palpation through the rectum.
Post-mortem findings include friable internal organs, abdominal effusion and evidence of sepsis in the joints, heart valves and brain.
Bacteria can usually be cultured from tissues collected at necropsy or identified by microscope examination.
Streptococcus species are the cause of opportunistic infections in poultry leading to acute and chronic conditions in affected birds. Disease varies according to the Streptococcal species but common presentations include septicaemia, peritonitis, salpingitis and endocarditis.
Common species affecting poultry include:
- "S. gallinaceus" in broiler chickens
- "S. gallolyticus" which is a pathogen of racing pigeons and turkey poults
- "S. dysgalactiae" in broiler chickens
- "S. mutans" in geese
- "S. pluranimalium" in broiler chickens
- "S. equi subsp. zooepidemicus" in chickens and turkeys
- "S. suis" in psittacine birds
The prodromal symptoms are fever, headache, and myalgia, which can be severe, lasting as long as 24 hours. After 1–5 days, typically, these are followed by diarrhea (as many as 10 watery, frequently bloody, bowel movements per day) or dysentery, cramps, abdominal pain, and fever as high as 40 °C (104 °F). In most people, the illness lasts for 2–10 days. It is classified as invasive/inflammatory diarrhea, also described as bloody diarrhea or dysentery.
There are other diseases showing similar symptoms. For instance, abdominal pain and tenderness may be very localized, mimicking acute appendicitis. Furthermore, "Helicobacter pylori" is closely related to Campylobacter and causes peptic ulcer disease.
Acute adenoiditis is characterized by fever, runny nose, nasal airway obstruction resulting in predominantly oral breathing, snoring and sleep apnea, Rhinorrhea with serous secretion in viral forms and mucous-purulent secretion in bacterial forms. In cases due to viral infection symptoms usually recede spontaneously after 48 hours, symptoms of bacterial adenoiditis typically persist up to a week. Adenoiditis is sometimes accompanied by tonsillitis. Repeated adenoiditis may lead to enlarged adenoids.
Complications include toxic megacolon, dehydration and sepsis. Such complications generally occur in young children (< 1 year of age) and immunocompromised people. A chronic course of the disease is possible; this disease process is likely to develop without a distinct acute phase. Chronic campylobacteriosis features a long period of sub-febrile temperature and asthenia; eye damage, arthritis, endocarditis may develop if infection is untreated.
Occasional deaths occur in young, previously healthy individuals because of blood volume depletion (due to dehydration), and in persons who are elderly or immunocompromised.
Some individuals (1–2 in 100,000 cases) develop Guillain–Barré syndrome, in which the nerves that join the spinal cord and brain to the rest of the body are damaged, sometimes permanently. This occurs only with infection of "C. jejuni" and "C. upsaliensis".
The proximity of the brain to the sinuses makes the most dangerous complication of sinusitis, particularly involving the frontal and sphenoid sinuses, infection of the brain by the invasion of anaerobic bacteria through the bones or blood vessels. Abscesses, meningitis and other life-threatening conditions may result. In extreme cases the patient may experience mild personality changes, headache, altered consciousness, visual problems, seizures, coma and possibly death.
Sinus infection can spread through anastomosing veins or by direct extension to close structures. Orbital complications were categorized by Chandler et al. into five stages according to their severity (see table). Contiguous spread to the orbit may result in periorbital cellulitis, subperiosteal abscess, orbital cellulitis, and abscess. Orbital cellulitis can complicate acute ethmoiditis if anterior and posterior ethmoidal veins thrombophlebitis enables the spread of the infection to the lateral or orbital side of the ethmoid labyrinth. Sinusitis may extend to the central nervous system, where it may cause cavernous sinus thrombosis, retrograde meningitis, and epidural, subdural, and brain abscesses. Orbital symptoms frequently precede intracranial spread of the infection . Other complications include sinobronchitis, maxillary osteomyelitis, and frontal bone osteomyelitis. Osteomyelitis of the frontal bone often originates from a spreading thrombo-phlebitis. A periostitis of the frontal sinus causes an osteitis and a periostitis of the outer membrane, which produces a tender, puffy swelling of the forehead.
The diagnosis of these complications can be assisted by noting local tenderness and dull pain, and can be confirmed by CT and nuclear isotope scanning. The most common microbial causes are anaerobic bacteria and "S. aureus". Treatment includes performing surgical drainage and administration of antimicrobial therapy. Surgical debridement is rarely required after an extended course of parenteral antimicrobial therapy. Antibiotics should be administered for at least 6 weeks. Continuous monitoring of patients for possible intracranial complication is advised.
Complications of acute adenoiditis can occur due to extension of inflammation to the neighboring organs.
The vegetations are small and formed from strands of fibrin, neutrophils, lymphocytes, and histiocytes. The mitral valve is typically affected, and the vegetations occur on the ventricular and atrial surface of the valve. Libman–Sacks lesions rarely produce significant valve dysfunction and the lesions only rarely embolize. However, there is data to suggest an association between Libman–Sacks endocarditis and a higher risk for embolic cerebrovascular disease in people with systemic lupus erythematosus (SLE).
There are several paired paranasal sinuses, including the frontal, ethmoidal, maxillary and sphenoidal sinuses. The ethmoidal sinuses are further subdivided into anterior and posterior ethmoid sinuses, the division of which is defined as the basal of the middle turbinate. In addition to the severity of disease, discussed below, sinusitis can be classified by the sinus cavity which it affects:
- Maxillary – can cause pain or pressure in the maxillary (cheek) area ("e.g.," toothache, or headache) (J01.0/J32.0)
- Frontal – can cause pain or pressure in the frontal sinus cavity (located above eyes), headache, particularly in the forehead (J01.1/J32.1)
- Ethmoidal – can cause pain or pressure pain between/behind the eyes, the sides of the upper part of the nose (the medial canthi), and headaches (J01.2/J32.2)
- Sphenoidal – can cause pain or pressure behind the eyes, but often refers to the skull vertex (top of the head), over the mastoid processes, or the back of the head.
Antibiotic misuse, sometimes called antibiotic abuse or antibiotic overuse, refers to the misuse or overuse of antibiotics, with potentially serious effects on health. It is a contributing factor to the development of antibiotic resistance, including the creation of multidrug-resistant bacteria, informally called "super bugs": relatively harmless bacteria (such as staphylococcus, enterococcus and acinetobacter) can develop resistance to multiple antibiotics and cause life-threatening infections.
The pathology is the same as nonbacterial thrombotic endocarditis except focal necrosis with hematoxylin bodies can be found only in Libman–Sacks endocarditis.
Marantic vegetations are often associated with previous rheumatic fever.
Other risk factors include:
- hypercoagulable states
- malignant cancers, especially mucin-producing adenocarcinomas (most commonly associated with pancreatic adenocarcinomas)
- systemic lupus erythematosus: Referred to as Libman-Sacks endocarditis
- trauma (e.g., catheters)
Grossly, vegetations form along lines of valve closure and are generally symmetric with a smooth or verrucoid (warty) texture. Histologically, lesions are composed of fibrin (eosinophilic) and platelets but, unlike bacterial etiologies, contain little evidence of PMNs, microorganisms or inflammation.