number Done by Corrected by Doctor Hamed Al Zoubi

Transcription

1 number 17 Done by Ensherah Mokheemer Corrected by Waseem Abu Obeida Doctor Hamed Al Zoubi

2 Today we are going to talk about the last two bacteria in this course which are Mycoplasma and Rickettsia. Let s begin. Mycoplasma and Ureaplasma Family: Mycoplasmataceae Genus: Mycoplasma Genus: Ureaplasma Species: M. pneumoniae Species: U. urealyticum M. hominis M. genitalium Morphology and Physiology: Mycoplasma species are the smallest free-living bacteria ( µm) Require complex media for growth, PPL4 PPL4 (PPLO), or pleuropneumonia-like organism: PPLO Selective Media are highly nutritious due to the addition of beef heart infusion, peptone supplemented with yeast extract and inactivated horse serum. Yeast extract provides diphosphopyridine nucleotides and serum provides cholesterol and a source of protein. Facultative anaerobes (can survive without oxygen), except M. pneumoniae, it is a strict aerobe. It lacks a cell wall which means that they are unaffected by many common antibiotics such as penicillin or other beta-lactam antibiotics that target cell wall synthesis. (Intrinsic/ inherent drug resistance (no target site)). It is Part of the normal flora: Respiratory tract flora: Mycoplasma pneumoniae Urogenital tract flora: Mycoplasma genitalium, Mycoplasma hominis, Ureaplasma urealyticum. Cytoplasmic and cell membrane rich in cholesterol and GLYCOLIPIDS

3 **Extra info: Mycoplasmas incorporate large quantities of cholesterol into their plasma membrane from their host or from the serum component of artificial growth media(ppl4). The presence of sterols in membrane helps in regulation of membrane fluidity P1 antigen in M. pneumoniae, which is involved in attachment and adhesion. P1 antigen has receptors on RBCs when binding it causes haemolysis of the RBCs causing haemolytic anaemia, so when you have a patient with pneumoniae and he has haemolytic anaemia think of Mycoplasma pneumonia. Fried egg like colonies Pathogenesis: P1 pili (M. pneumoniae) When doing a respiratory CBC (*complete blood count) test to a patient with Mycoplasma pneumoniae infection we notice a decrease in the Haemoglobin level due to haemolytic anaemia which increases the breakdown of haemoglobin and leads to an increase in the bilirubin level. *Complete blood count: is a panel of tests that evaluates the three types of cells that circulate in the blood Movement of cilia ceases: Attachment of the bacteria to host cells can result in loss of cilia movement which will cause the loss of the clearance in the respiratory tract leading to the entry of foreign bodies and reaching the lungs and causing inflammation and airway dysfunction. Clearance mechanism stops resulting in cough glycolipids Brain cells cross antigenicity: The glycolipids of the mycoplasma looks like the glycolipids which are present in the brain cells so the antibodies which are formed against these glycolipids(mycoplasma s) will cross react with the glycolipids present in our brain cells affecting the central nervous system. Diseases Caused by Mycoplasma:

4 Organism Disease M. pneumoniae Upper respiratory tract disease, tracheobronchitis, atypical pneumonia, (chronic asthma??) M. hominis Pyelonephritis, pelvic inflammatory disease, postpartum fever M. genitalium Nongonococcal urethritis U. urealyticum Nongonococcal urethritis, (pneumonia and chronic lung disease in premature infants??) Now let s discuss the underlined terms: -Atypical pneumonia: is a type of pneumonia that is not caused by the traditional pathogens of typical pneumonia. The pathogens responsible for atypical pneumonia are Chlamydophila pneumoniae, Mycoplasma pneumonia, Legionella pneumophila, Moraxella catarrhalis. * It could be bacteria, fungi, protozoa or viruses *It produces Sputum that is either mild or absent and produces non-productive cough. Extra info: Typical pneumonia is: * primarily bacterial, it may be viral; Streptococcus pneumoniae, Staphylococcus aureus, Escherichia coli, and Haemophilia influenzae *It produces Bulk sputum with productive cough. -Chronic Asthma: Infections with M. pneumoniae can precede the onset of asthma, exacerbate asthmatic symptoms, and cause difficulties with asthma management. But, the role of M. pneumoniae as the cause of the initial onset of asthma remains unclear. -Pyelonephritis: The doctor illustrated the difference between Pyelonephritis and cystitis briefly. Cystitis: an infection of the bladder or urethra (Below the kidney), Pyelonephritis: an infection which involves the bladder and urethra, and whose damage extends up to the ureters and kidneys (Above the kidney). (More details later in the urology course). -Nongonococcal Urethritis: Nongonococcal urethritis (NGU) is an inflammation of the urethra that is not caused by gonorrhoeal infection. Gonorrhoeal infection: is a sexually transmitted infection (STI) caused by the bacterium Neisseria gonorrhoeae. Scientists usually put gonorrhoeal infections as a separate category. U. urealyticum: Ureaplasma urealyticum has an etiological role in the development of infection stones in the urinary tract, U. urealyticum causes alkalinisation of the urine by

5 producing urease which splits the urea leading to an Alkaline media that induces the precipitation of stones. Mycoplasma pneumonia: It causes: -Tracheobronchitis -Atypical pneumonia (walking pneumonia) Walking pneumonia is a bacterial infection that affects your upper and lower respiratory tract. It s also called atypical pneumonia, because it s usually not as severe as other types of pneumonia (as mentioned before). It doesn t cause symptoms that require bed rest or hospitalization. It might just feel like a common cold and can go unnoticed as pneumonia. Most people can carry on with their daily lives. This type of pneumonia is considered atypical since the cells causing the infection are resistant to penicillin, the drug that is normally used to treat pneumonia. Epidemiology: Occurs worldwide (common in the age of children until collage age) No seasonal variation Proportionally higher in summer and fall (to the beginnings of winter) Clinical Syndrome: Incubation 2-3 weeks Fever, headache and malaise Persistent non-productive cough Non-productive cough: it is a cough that does not bring up any mucus. It is also known as dry cough. Respiratory symptoms - Radiological signs precede symptoms: the signs of atypical pneumonia such as infiltration appears in the X-Ray before the symptoms and the physical signs start to show on the patient. Slow resolution Even after treatment with the right antibiotic x-ray might show remaining infiltration and radiographic abnormalities. Slow or incomplete resolution of pneumonia despite treatment is a common clinical problem. Rarely fatal

6 Laboratory Diagnosis: The diagnosis of Mycoplasma Pneumonia is usually clinical, and it depends on the doctor, because laboratory diagnosis is difficult and takes long time. When you have a patient with pneumonia (unknown etiology) give him antibiotic therapy that covers both typical and atypical pneumonia until the lab results come out if it is Streptococcus pneumoniae for example (typical pneumonia) stop the atypical therapy and continue with the typical treatment. Microscopy Difficult to stain Can help eliminate other organisms Culture (definitive diagnosis) May take 2-3 weeks Serology A four-fold or greater rise in antibody titre, with a peak at about 3 4 weeks, is indicative of a recent M. pneumoniae infection. Patients infected shows an increase in antibody titers (2-fold increase of serum M. pneumoniae IgM or a 4-fold increase in M. pneumoniae IgG), Titres > 16 of IF IgA are specific for Mycoplasma infection. *Extra info, Fold change: is a measure describing how much a quantity changes going from an initial to a final value. For example, an initial value of 30 and a final value of 60 corresponds to a fold change of 2. PCR Treatment and Prevention: Antibiotics that inhibits cell wall synthesis like penicillin and vancomycin, do not work against Mycoplasma Pneumonia since it does not have cell wall. Treatment Tetracycline or erythromycin Newer fluoroquinolones Can t use cell wall synthesis inhibitors

7 Prevention Avoid close contact No vaccine Rickettsia and Orientia Small obligate intracellular parasites Once considered to be viruses (Because it is intracellular) Gram-negative bacteria Stain poorly with Gram stain (we use Giemsa) Reservoirs - animals, insects and humans Reservoirs: is the habitat where an infectious agent is naturally found, it is where it grows, multiplies and where it does not cause illness or disease. Arthropod vectors Vectors: any agent that carries and transmits an infectious pathogen into another living organism. Organism Disease Vector Reservoir R. rickettsia Rocky Mountain Tick Ticks, rodents Spotted fever O. tsutsugamushi Scrub typhus Mite Mites, rodents R. prowazekii Epidemic typhus Louse Humans, squirrel fleas R. thypi Murine typhus Flea Rodents )القراد( cattles. *Ticks: they are present on cats, dogs, and some )البراغيث( *fleas: )العث( *Mites: )القوارض *Rodents:) Replication of Rickettsia and Orientia: Infect endothelial in small blood vessels - Induced phagocytosis but it escapes phagocytosis either by acidic changes or envelops but these are just theories the real mechanism is still unknown. Lysis of phagosome and entry into cytoplasm Phospholipase (to mediate entry into the host cell, escape from the phagosome, and cause injury to host cells by both typhus and spotted fever group rickettsia.)

8 Replication (within the cytoplasm of a eukaryotic host cell) Release (The host cell then lysis and releases the rickettsia progeny to initiate a new infection cycle.) -When the new rickettsia is released it is released either by budding or by cell lysis (similar to viruses) -It destroys endothelial cells which is the cause of the rash. Spotted Fever Group: -Caused by Rickettsia rickettsia -Main clinical feature is spotted fever (rash and fever) -Vector: Tick Rocky Mountain Spotted Fever - Incubation period 2 to 12 days - Abrupt onset fever, chills, headache and myalgia - Rash appears 2-3 days later in most (90%) patients Begins on hands and feet and spreads to trunk (centripetal spread). Palms and soles common. Maculopapular but can become petechial or haemorrhagic. - Complications from widespread vasculitis Gastrointestinal, respiratory, seizures, coma, renal failure Most common when rash does not appear -Fatal complications when it reaches the brain and the heart -Mortality in untreated cases - 20%

9 Laboratory Diagnosis: Initial diagnosis - clinical grounds Direct Fluorescent Ab (Antibody) test for Ag (Antigen) in punch biopsy (skin biopsy) - reference labs PCR based tests - reference labs Serology Indirect fluorescent Antibody test for Antibody Latex agglutination test for Antibody Extra info: Direct Immunofluorescence uses a single antibody directed against the target of interest. The primary antibody is directly conjugated to a fluorophore. Indirect Immunofluorescence uses two antibodies. The primary antibody is unconjugated, and a fluorophore-conjugated secondary antibody directed against the primary antibody is used for detection. Treatment and Prevention: Tetracycline (The drug of choice for treating rickettsial infections of all types and in all age groups is doxycycline.) Prompt treatment reduces morbidity and mortality No vaccine Prevention of tick bites (protective clothing, insect repellents) Prompt removal of ticks Can t control the reservoir Typhus Group: (Rickettsia typhi and Epidemic typhus) -caused by Rickettsia prowazekii -Vector: Louse -It causes: Epidemic typhus: a form of typhus so named because the disease often causes epidemics following wars and natural disasters. It is the only one in which humans are considered as a reservoir.

10 Brill-Zinsser disease: when epidemic typhus relapses again it is called Brill- Zinsser and it is usually mild, less severe, than the epidemic typhus and with lower mortality rate. Epidemic typhus: Incubation period approximately 1 week Sudden onset of fever, chills, headache and myalgia After 1-week rash: Maculopapular progressing to petechial or haemorrhagic First on trunk and spreads to extremities (centrifugal spread) Complications Myocarditis, stupor, delirium (Greek typhus = smoke) Recovery may take months Mortality rate can be high (60-70%) Laboratory Diagnosis: Isolation possible but dangerous Serology Treatment: Tetracyclines. Rickettsia typhi: Causes Murine or endemic typhus: (Murine means rats) It is a form of typhus transmitted by rat s flea, usually on rats. (This contrasts with epidemic typhus, which is usually transmitted by lice.) Epidemiology: Occurs worldwide Vector - rat flea Bacteria in feces Reservoir - rats No transovarian transmission

11 Transovarial transmission: occurs in certain arthropod vectors as they transmit diseasecausing pathogens from parent arthropod to offspring arthropod. Rickettsia prowazekii is not passed on by transovarian transmission because it kills the vector that carries it. Normal cycle - rat to flea to rat Humans accidentally infected Clinical Syndrome: Incubation period 1-2 weeks Sudden onset of fever, chills, headache and myalgia Rash in most cases Begins on trunk and spreads to extremities (centrifugal spread) Mild disease - resolves even if untreated Laboratory Diagnosis: Serology Indirect fluorescent antibody test Treatment: Doxycycline The End Sorry for any mistake Don t hesitate to contact me if you have any questions Good Luck