6 Microbiology Carditis Dr.mohamed shakkeeb 17/3/2016 Hothaifa Alshoqran

Transcription

1 6 Microbiology Carditis Dr.mohamed shakkeeb 17/3/2016 Hothaifa Alshoqran

2 Hello guys :"3 According to Dr. Shakeeb the slides are enough for the exam and the questions will not include anything out of the slides, so I just rearranged them with some notes. We will only take one Microbiology lecture in this system. In this lecture, we will discuss microbiology of carditis. The focus will be on this :$ Microbiology of carditis Infective endocarditis Myocarditis Pericarditis **we will talk about the etiology without going into details Infective endocarditis: It is a serious infection mandating prompt diagnosis and intervention (i.e., it requires correct diagnosis), so it is an emergent condition and it is described by Bulky, friable vegetation composed of necrotic debris, thrombus, and organisms result from Microbial invasion of heart valves or mural endocardium. So the main event in infective endocarditis is vegetation and it mainly happens on the valves and endocardium but could also form on the aorta or blood vessels or prosthetic devices such as artificial valves and pacemakers. This is how vegetation looks like P a g e 1

3 The main cause for infective endocarditis is extracellular bacteria but other organisms can also be responsible for it, such as fungi, rickettsiae (agents of Q fever), and Chlamydial species. We can classify Infective endocarditis based on the tempo and severity of the clinical course. It may be acute or sub-acute (other sources say that there is a chronic form as well, but it is not important for us). The acute form Refers to a severe, destructive infection, frequently involving a highly virulent organism and mainly attacks a normal valve. Very highly virulent, like Staph. Aureus and affected normal valve will be the clinical picture to those who have acute endocarditis. And it will be a rapid course. Capable of causing substantial morbidity and mortality even with appropriate antibiotic therapy and/or surgery. Sub-acute refers to infection by organisms of low virulence and involves previously abnormal heart or abnormal heart valve such as a calcified, scarred or deformed valves, and this form appears insidiously and follows a protracted course of weeks to months. Most patients recover after appropriate antibiotic therapy unless they had the acute form which has a destructive effect even if antibiotics were used for therapy. Pathogenesis Infective endocarditis can develop on previously normal valves, but cardiac abnormalities predispose to such infections. Those that predispose the infection are: P a g e 2

4 1- Rheumatic heart disease 2- Mitral valve prolapse 3- Bicuspid aortic valves 4- Calcific valvular stenosis Statistics indicate that Prosthetic heart valves now account for 10% to 20% of all cases of infective endocarditis. Now the most important feature of the disease or infection is the deposition of sterile platelet-fibrin at sites of pacemaker lines and these deposits are actually foci for bacterial seeding with subsequent development of endocarditis. Also, indwelling vascular catheters, and damaged endocardium due to jet streams caused by pre-existing cardiac disease can be foci for bacterial seeding with subsequent development of endocarditis. Neutropenia There are some Host factors that increase Immunodeficiency the risk of infective endocarditis, as well as adversely affecting outcomes, these are: Malignancy The causative organisms differ depending on risk factors and the underlying abnormality. What does this means? Example: 50% to 60% of the cases of endocarditis occurring on damaged or deformed valves are caused by Streptococcus viridans. By contrast, the more virulent S. aureus can attack deformed valves but mainly attacks healthy valves and is responsible for 10% to 20% of the cases overall. S. aureus is the major offender in infections occurring in intravenous drug abusers. Diabetes mellitus Alcohol Intravenous drug abuse The Dr. focused on this point and said that it is very important especially in studying internal medicine and surgery in the clinical years as infective endocarditis will be presented frequently in the ER. Hence it is important to know that the cause of the disease in drug abusers is S.aureus. P a g e 3

5 -There are additional bacterial agents that can cause infective endo. And these include enterococci and the so-called HACEK group (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella). -"HACEK group" need very special conditions to grow in the lab. -Enterococci and HACEK group are commensal in the oral cavity, in certain conditions these MOS will reach the blood stream and cause inf. Endocarditis. -More rarely, gram-negative bacilli and fungi are involved. In some cases of inf. Endocarditis we won t be able to isolate MOs from the blood. We call this case "culture-negative" endocarditis. The reason behind that may be : Previous antibiotic therapy. Deeply embedded organisms within the enlarging vegetation are not released into the blood. Difficulties in isolating the offending agent. E.g Chlamydia, coccidian. These MOs are difficult to be isolated in the lab. Foremost among the factors predisposing to endocarditis is seeding of the blood with microbes. But how could MOs enter the blood? 1-Having pneumonia may lead to bacteremia as a complication. This also happens in GI or UTI infection. 2-A dental or surgical procedure that causes a transient bacteremia. This is why a dentist gives us an antibiotic before having a dental procedure. This is for prophylaxis in order to prevent infection as the oral cavity is full of MOs that may enter the blood stream. And if this happens in a person having predisposing factors this will cause endocarditis. So the persons who have artificial heart valves must follow prophylactic antibiotics before doing any minor or major surgery. P a g e 4

6 3-Injection of contaminated material directly into the blood stream by intravenous drug users. 4-An occult source from the gut or the oral cavity. E.g: abscess will allow MOs to reach the blood stream and cause the infection. As we already said, Recognition of predisposing anatomic substrates (artificial valves) and clinical conditions causing bacteremia allows appropriate antibiotic prophylaxis. Morphology of IE In both acute and sub-acute forms of the disease, friable, bulky, and potentially destructive vegetations containing fibrin, inflammatory cells, and microorganisms and platelets are present on the heart valves. The aortic and mitral valves are the most common sites for infection. But in intravenous drug abuse the most common site is the tricuspid valve. Vegetations may be single or multiple and may involve more than one valve. The vegetations can sometimes erode into the underlying myocardium to produce an abscess cavity (ring abscess). We already said that vegetations. are fragile so sometimes there may be Shedding of emboli from them. This emboli will then go to any site in the body (the brain, the liver, etc) causing an abscess because they contain a large amount of MOs. -Sub-acute endocarditis typically elicits less valvular destruction than that associated with acute endocarditis. -On microscopic examination, the sub-acute vegetations of infective endocarditis often have granulation tissue at their bases. Dr did not read this >>> promoting development of chronic inflammatory infiltrates, fibrosis, and calcification over time. P a g e 5

7 Multiple vegetations Ring abscess Signs and symptoms of IE Fever is present in 90% of patients with IE. Heart murmurs are heard in approximately 85% of patients. Also, one or more classic signs of IE are found in as many as 50% of patients. They include the following: 1-Petechiae 2-Subungual (splinter) hemorrhages: Dark-red, linear lesions in the nail beds. P a g e 6

8 3-Osler nodes: Tender subcutaneous nodules usually found on the distal pads of the digits. 4-Janeway lesions: Non-tender maculae on the palms and soles. 5-Roth spots: Retinal hemorrhages with small, clear centers; rare and observed in only 5% of patients. Signs of neurologic disease: Again, we said that vegetation is fragile and the most common phenomena in IE is embolus formation, and this embolism may lead to: Embolic stroke with focal neurologic deficits: The most common neurologic sign. Multiple micro-abscesses Intracerebral hemorrhage *Dr said we may have a question in the exam about the signs and symptoms so memorize them well. -Lab diagnosis: The Duke (a scientist) worked with his colleagues and developed a criteria to diagnose IE. P a g e 7

9 The criteria depend on the clinical picture and on the microbiologic, pathologic and echocardiographic characteristics of a specific case. Major blood culture criteria for IE include: Major echocardiographic criteria include the following: Two blood cultures positive for organisms typically found in patients with IE. "There is more than one but the Dr. only put this in the slides". Echocardiogram positive for IE. -Myocardial abscess. -Development of partial dehiscence or detachment of a prosthetic valve. When we have an infection, the invader MOs cause detachment of the valve from its original place. -New-onset valvular regurgitation Minor criteria for IE include the following: -Predisposing heart condition or intravenous drug use. -Fever of 38 C (100.4 F) or higher. -Vascular phenomenon, including major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhage, or Janeway lesions. -Immunologic phenomenon such as glomerulonephritis, Osler nodes, Roth spots, and rheumatoid factor. -Sometime Echocardiogram results consistent with IE but not meeting major echocardiographic criteria (We see a positive result in Echo. But these results differ from the four major criteria so here we consider this result a minor criteria). Now by knowing these criteria we can diagnose IE if we found one of these conditions in the patient: 2 major criteria. 1 major criterion and 3 minor criteria. 5 minor criteria.. So the detection of any one of these 3 conditions will diagnose IE. P a g e 8

10 Treatment Treatment should be based on anti-microbial susceptibility test in the lab that is made on MOs isolated from the blood in order to decide what should be used. -But mainly Viridans streptococci were the most common MOs isolated and are susceptible to penicillin. So penicillin is the drug of choice here. -We usually use Bactericidal therapy by combining penicillin with an aminoglycoside. -For the prevention of bacterial endocarditis in patients at risk following dental extraction, the dentist gives 3g of amoxicillin orally 1 h before the procedure. -Anti-staphylococcal antibiotic, we use Flucloxacillin as the drug of choice and sometimes vancomycin is used. -Enterococci: amoxicillin +gentamicin (synergic effect). -HACEK: amoxicillin +gentamicin. **Although some books say that third generation of cephalosporin is the drug of choice for HACEK but keep in mind what the Dr said. -In culture-negative IE we diagnose the MOs by serological evidence which is made by looking at specific antibodies as it is difficult to isolate the organisms in the lab, and the MOs that usually cause this infection is coxiella burnetti and Chlamydia and it is very important to diagnose them as they are susceptible to tetracycline which is the drug of choice here. P a g e 9

11 Myocarditis Is an inflammation of the myocardium and most cases are viral. There s evidence that up to 20% of the cases of idiopathic dilated cardiomyopathy have myocarditis. Myocardial injury may be a consequence of Direction damage by an infectious agent and then inflammation. e.g.: brucellosis, meningococcal, streptococcal and staphylococcal sepsis, Legionella spp, M.pneumoniae, C.psittici infection. By circulating toxins. e.g.: C.diptheriae and C.perfringens. These bacteria secrete toxins which is toxic to the cardiac muscle and renal tissue. Etiology By immune reaction following an infection. e.g.: Lyme disease, acute rheumatic fever. -In most cases the cause is not identified. -Viruses are the commonest agents in developed world, e.g. Measles, influenza,polio, mumps adenoviruses, and group B Coxsacki viruses. -Parasitic causes include T.cruzi which is a common cause in South America. -Disseminated infection in the immunocompromised may lead to myocarditis (Toxoplasma, Aspergillus and Cryptococcus spp). P a g e 10

12 Pericarditis An inflammation of the pericardium which may be acute or chronic. Viruses: - enteroviruses particularly coxsackie viruses are the commonest cause. -Others include Ecoviruses, adenovirus, mumps, influenza, EBV, Varicilla, CMV, HSV and hepatitis B virus. Parasite: includes Toxoplasma gondii,entamoeba histolytica Etiology Fungi: Includes Histoplasma capsulatum, Aspergillus spp, Cryptococcus neoformans, candida spp. Bacteria: -before antibiotics became widely available, bacterial pericarditis staphylococcus aureus streptococcus pneumoniae was recognized as complication of pneumonia. -bacterial pericarditis is now uncommon and tends to occur following a gram-negative infection in older people with a predisposing condition like esophageal perforation, head and neck infections (anaerobes), and in some cases of meningococcal septicemia. -Other bacteria causes include mycoplasma pneumoniae, Legionella pneumophila, haemophilus influenza. -Tuberculosis pericarditis is a major cause of heart failure in sub-saharan Africa, chronic disease is associated with constrictive pericarditis The end P a g e 11

13 بين جهاز قد مضى و جهاز على الطريق آت... تتزاحم اختبارات و محاضرات تمأل الطريق!!!,,, نحن ما زلنا نحن باشكالنا و اسمائنا الهيئة هي نفسها الهيئة ولكن..!!! بعزيمة و ق لب جديد..! ولدنا من جديد.. :"( مع همة تعانق السحاب... باحثة عن ذات لطالماحلمنا بها صغارا... و اليوم ها نحن نرسم بداياتها تو اقين لجني ثمرات التعب.....ببسمة طف ل و دعوة أم قد استشعروا بين اكفنا رحمةاالله... فيا رب وفقنا في طريقنا حملة لهذه الرسالة العظيمة و يس ر لنا كل عسير... و آخر دعواناان الحمدهلل رب العالمين. Edited by: Salam Mustafa P a g e 12