"Atypical" Bacteria: Mycoplasma, Ureaplasma, Mycobacteria Flashcards
Mycobacterium
Gram positive “ghosts,” acid fast positive.
They have a cell wall, but it is made up of different components and does not allow good staining.
Commonly found in water and soil
Infections: lung, skin and soft tissue, lymph nodes, GI tract, other… if it can get into the space they will lead to an infection.
Nontuberculosis Mycobacteria: Mycobacterium avium-intracellulare (MAI); primarily a disease of HIV/AIDS; many others.
Live in water
All mycobacterium; replicate at a much slower rate than other bacteria.
Slow metabolizers, do not like to live in a fast world.
Just as difficult to treat as M. tubecurlosis.
Do not grow so very hard to culture in the lab.
M. Tuberculosis
Mycobacterium
-Aerobic, non-spore forming, non-motile bacillus
-High cell wall lipid content; high lipid characteristic of cell wall, not peptidoglycan.
S.aureus has a turnover rate of 30 minutes, for reference.
-Slow growing 15-20 hour turnover
-Carried in airborne particles
-10% infection risk with + PPV.
-Multi-drug resistance prevalent.
Historically significant pathogen
Humans are the only reservoir for the species
Consumption: actors, poets, writers depiction of disease in 19th century.
Not identified as contagious until 1882 by Dr. Robert Koch; started the germ theory of disease (bacteria cause infection and ways to treat these infections),
Patients wither away over the time, cough up blood, lose weight, night sweats=consumption type disease.
Isolated patients, knew it was transmitted between people; this prevented the spread.
Strange treatment theory.
Sensitive to UV light; if exposed to sun it would die.
Does not cause much disease in the US.
9 million people in the world have active TB (2011) (active infection).
MDR and XDR (greater than or equal to 3 drugs resistance) TB in the US.
Worldwide health problem:
1/3 of the worlds population are infected with TB (2-3 billion)
TB is a leading killer of people living with HIV.
Reported TB in the US:
1953: 52.6/100,000 population; 12.4% death
2010: 3.6/100,000 population; 0.2% death.
High rates of HIV and TB; subsahran Africa and east/southeast asia.
Risks for antibiotic resistance in TB
- Exposure to a person who has known drug resistant TB
- Exposure to a person wiht active TB who has had prior treatment for TB (treatment failure or relapse) and whose susceptibility test results are not known.
- Exposure to persons with active TB fro areas in which there is a high prevalence of drug resistance; southeast Asia and Saharan Africa.
- Exposure to person who continue to have positive sputum smears after 2 months of combination chemotherapy; should be still having some containment.
- Travel in an area of high prevalence of drug resistance.
M. tuberculosis identification
Culture is the gold standard for detection but may take weeks to grow; Mtb can take a couple months to grow and 20 hours to replicate one cell.
But culture=identification.
-Antibiotic susceptibility testing is difficult; hard because you have to culture and then ID the resistance markers in the organism.
-Acid-fast bacilli=mycobacteria; stain of smear and see if positive based on reaction of organism and acid; some sort of mycobacterium species.
-Mtb can be detected in any biologic fluid
-QuanterFERON gold; detection of latent and active Mtb; not gold standard; serum test; detects interfeurons released from WBC; this is specific for TB to see if patients have active disease.
Latent Mtb
Infected (alive bacteria, not active).
Skin test or blood test result indicating TB infection.
Normal chest XRay and negative sputum test.
No symptoms of disease
Not contagious
Requires a single drug treatment (one antibiotic); 3-5% risk of active Mtb in year 1; 5% lifetime risk of active Mtb thereafter; treatment lowers lifetime risk to <1%.
Active Mtb
Infected (alive bacteria, active)
Skin test or blood test results indicating TB infection.
Abnormal chest xray or positive sputum smear or culture; infiltrate or nodule that indicate TB on XRAY.
Symptoms of disease coughing, fever (night sweats), and weight loss.
Contagious
Requires multi-drug treatment.
TB vaccine
Bacillus Calmette-Guerin (BCG) vaccine
Live-attenuated strain of M. bovis; non mycobacterium species.
Done in countries with high endemic rates of TB.
Often used in young children throughout much of the world with high TB prevalence
Used to develop an immune response to be able to prevent activation of disease in patients..
60-80% decrease in disease.
Does not prevent infection, but does often prevent progression to clinical disease.
Effectively prevents disseminated disease in young children.
Increases likelihood of positive PPD because you will have an immune response to TB.
Drug resistant TB
Resistance to Isoniazid (INH)
Some is multidrug resistant showing resistance to at least INH and rifampicin; 2 essential first line drugs.
XDR is MDR TB plus resistance to fluoroquinolones and to any of the three second line injectable agents (amikacin, kanamycin, capreomycin).
10% risk of drug resistant TB in US.
1% in US are MDR and <1% are XDR TB.
7% are INH resistant.
CDC rates this as serious.
Antibiotic targets and resistance in Mtb
Combination approach using multiple mechanisms of action.
Multiple targets to counteract slow growing organisms.
Target many things within bacteria to counteract active infection.
First line treatment of TB for Drug sensitive TB:
Isoniazid
Rifampin
Ethambutol
Pyrazinamide
in combination that we know work for TB.
I, E, and P we think inhibit cell wall synthesis; maybe works on ATP synthesis.
Rifampin inhibits RNA synthesis through RNA polymerase.
MDR TB;
KO 2 classes of agents; isoniazid and rifampin which are the backbone of TB therapy.
Add flouroquinolones (inhibits DNA gyrase) and aminoglycosides (inhibits protein synthesis), PAS (inhibits synthesis if DNA precursors), cyclic peptides (inhibits protein synthesis), thioamides, cycloserine (the last 2 acting on cell wall synthesis); but limited.
XDR TB:
Isoniazid, rifampin, flouroquinolines are all resistant in this example.
Non-TB Mycobacteria
Seen in immunocompromised hosts.
Primary component of morbidity and mortality in HIV patients in the US.
Blood stream infections
Often combination therapy.
M.avium-intracellulare (MAI)
-Environmental organism, relatively avirulent in the normal host
-Infection: pulmonary, systemic, and lymphadenitis (children), other sites less common.
-Prevention: 1 antibiotic; treatment: multiple.
-More than 120 species of nontuberculous mycobacteria (NMT),
-Environmental organism, common water source.
-M. fortuitum and M. abscessus common in skin/soft tissue, bone, and respiratory infections.
-Treatment often complicated and long.
Mycobacterium leprae; distribution of Leprosy in the US; transmitted by humans and armadillos.
Atypical in cell wall area; they do not have one!
MAC and MAI
HIV driven organism; if you have less than 50 WBC, active risk of infection and prophylax them.
Found in water, soil, and animals; not spread from person to person.
MAC causes pulmonary disease, lymphadenitis, and disseminated disease.
Pulmonary disesae occurs in older patients with COPD, prior pneumonia, and steroid use, as well as older women with no predisposing factors.
Lymphadenitis is mostly in children younger than 5 years old.
Dissmeinated disease: patients with AIDS and CD4 cell count less than 50/mm^3.
Clinical manifestations and diagnosis:
Pulmonary disease can be infiltrative with or without cavities, nodular (solitary or multinodular), pleural, or as a hypersensitivity pneumonitis. It can closely mimi TB. Diagnosis requires a triad of clinical symptoms, radiographic abnormalities and culture.
-Lymphadenitis is usually cervicofacial, unilateral, and painless. Diagnosis via lymph nose aspiration or excision.
Disseminated disease is usually accompnaied by fever, weight loss, and night sweats. Diagnosis is made in more than 90% of patients by blood cultures for M. avium complex (MAC).
Atypicals
2 of these are atypical; in cell wall area; they do not have a cell wall.
1. Legionella pneumophila
-“Legionnaires disease”
-Widespread in water; air cooling systems
-Actually a gram negative rod, not a true atypical
2. Chlamydophila pneumonia
-Often causes mild RTIs
-Actually a gram negative rod, not a true atypical
3. Mycoplasma pneumonia
-True atypical pathogen
-Outbreaks common in close contact.
-Seasonally associated
THESE ARE ATYPICAL PNEUMONIA=WALKING PNEUMONIA! 25% of Community Acquired Pneumonia (CAP)
4. Ureaplasma urealyticum; lower genital tract and urinary tract pathogen.
Z-pack covers all 3 of the atypical pneumonia class.
Legionella pneumophila
Legionnaire’s disease; named after a 1976 outbreak due to an outbreak at a Philadelphia convention of the American LEGION
2011-2015: CDC states that Legionella outbreaks are increasing.
-Treatment options: fluoroqunolones, macrolides, tetracyclines.
-Multiple outbreaks and modes of transmission; involved water.
Inhalation from air coolant systems and become infected that way.
Chlamydia pneumoniae
Obligate intracellular pathogen
Causes epidemics of CAP; military bases, schools, nursing homes.
Often cannot be differentiated from other CAP organisms.
Detected in clinic by: serologic testing to ID anti-C pneumoniae imunoglobulin G (IgG), IgA, and IgM antibodies; PCR testing and other rapid testing available.
Treatment: fluoroquinolones, macrolides, tetracyclines
Serologic test approved in US.
Goes right into next cell after replication, very hard to get out in culture.
Mycoplasma spp
Prokaryotes lacking a cell wall=no gram stain
Smallest known free living organism
Intracellular and extracellular pathogen
M. pneumoniae, M. pentrans, and M genitalium, M fermentans, and M hominis
Outbreaks in persons with close contact are commonly described for pneumonia
No cell wall therefore susceptible to non cell wall active AB; fluoroquinolones, macrolides, tetracyclines.
Also difficult to culture.
