RICKETTSIA RICKETTSIAE: Poorly staining gram-negative pleomorphic rods.
INTRACELLULAR VIRUS-LIKE THINGIES
RICKETTSIA RICKETTSIAE: Poorly staining gram-negative pleomorphic rods.
Family Properties: RICKETTSIACEAE
Strict Intracellular Parasites
Requirwe NAD and ATP for growth
OTHER SPECIES:
Ehrlichia: Arthropod-vectored infection of WBC's. No rash.
Coxiella: Q-Fever. Usually carried by farm animals.
RES involvement -- hepatosplenomegaly. Maybe no pneumonia.
No rash.
Epidemiology / At Risk: Found in the Eastern U.S., spread by ticks, in the Summer.
Manifestations: Rocky Mountain Spotted Fever is the best known example.
General Properties:
Arthropods are vectors.
They infect endothelial cells, starting with small capillaries and working their way up, leading to thrombosis and hemorrhage.
There is a prominent rash and fever.
Time Course:
4-7 days: Extensive rash, extending from extremities to trunk. Rash resembles Syphillus.
2 weeks: Very sick. High fever, DIC, hypotension, gram-negative shock.
Cardiac failure, renal failure, and encephalitis are likely causes of death.
OTHER RICKETTSIAL INFECTIONS:
Typhus: Several species and several vectors. Rash spreads from trunk to extremities, rather than RSMF which is the opposite.
Rickettsial Pox: From mites. Benign, self-limited rash.
Processing:
Specimen: Rash biopsy for RMSF.
Culture: Egg or tissue culture.
Identification:
Direct FA on endothelial cells
Serology: Indirect FA to measure antibody levels.
Antibody titer of 1:64, or Acute:Convelescent titer of 4X
Virulence:
Outer Membrane Proteins
Phospholipase: Acts as an invasin, helping bugs get into endothelial cells.
LPS: Strong endotoxic component.
Actin Polymerization: Making little projection to infect other cells. Some sort of way for the bugs to spread from cell to cell, similar to Shigella.
Host Immune Response: Probably combination of antibody plus cell-mediated. Not sure.
Vaccine / Prevention: Protective clothing.
Treatment: Tetracycline.
CHLAMYDIA TRACHOMATIS: Gram-negative rods.
Family Properties: CHLAMYDIACEAE
Obligate intracellular parasite
Tropic for columnar epithelia.
Gram-negative, but no peptidoglycan layer.
Dependent on ATP from host.
LIFE-CYCLE:
Elementary Body: Individual bugs living outside the host. They infect the host by endocytosis. They then multiply inside the host, utilizing host ATP.
Reticular Body: Cluster of bugs forming an inclusion body inside the cytoplasm of the host cell. They are released from the host-cell, to form more elementary bodies, which then go on to infect other cells.
Epidemiology / At Risk:
Leading cause of preventable blindness.
Leading cause of PID.
Manifestations:
Chronic Keratoconjunctivitis: Types A, B, C
Progressive conjunctivitis causes blindness by age 15 or 20.
Chlamydial Urethritis: Types D-K
So-called "Non-gonococcal urethritis."
PID
Inclusion Conjunctivitis (TRIC): Types D-K. Problem in newborns. Not the same as blindness above.
By law, (along with Gonococcus), newborns are treated prophylactically with eyedrops.
Lymphogranuloma Venereum: Types L1-L3.
Sexually transmitted, but the primary manifestation is suppurative (and later granulomatous) inflammation of inguinal lymph nodes.
Processing:
Specimen: Scrapings are taken for the inclusion conjunctivitis, UG, or rectal. Look for bugs in epithelial cells.
Stain: Giemsa stain. Iodine stain, looking for brown inclusion bodies.
Culture:
Identification:
Serotypes
A-C: Keratoconjunctivitris, found in Asia and Africa
D-K: Most prevelant in U.S. Urethritis and inclusion conjunctivitis.
L1-L3: Lymphogranuloma Venereum. Asia and Africa.
Iodine-Positive: Inclusion bodies contain a lot og glycogen and thus stain brown with iodine.
Virulence: Mostly focused on the Reticular Body.
ATPase: Helps the bug utilize the host cell's ATP.
ATP-ADP Translocase: In conjunction with the ATPase, this allows the bug to utilize the host cell ATP (high energy phosphate bonds) as a source of energy.
Cylindrical Projections: Little projections that probably help the bugs utilize host-cell nutrients.
LPS: Antigenic, providing a group-antigen for this bug.
Outer Membrane Proteins: Antigenic source for most of the serotyping (Types A-K, L1-L3).
Treatment: Tetracycline.
CHLAMYDIA PNEUMONIA: Gram-negative rods.
Manifestations: Walking Pneumonia, aka TWAR.
Infection of columnar epithelium of upper respiratory tract.
Identification: No processing usually needed. Disease can be treated based on clinical manifestation alone.
Treatment: Tetracycline.
CHLAMYDIA PSITTACI: Gram-negative rods.
Epidemiology / At Risk: Respiratory droplets inhaled. Found in pet birds (parrots, parakeets), poultry birds. People talking to their birds up close, etc.
Manifestations: Psitaccosis. An interstitial pneumonia.
Headache (can be severe), and dry, non-productive, hacking cough.
Sequelae: severe headache, encephalopathy, possible convulsions, coma, and death.
Processing:
Specimen: Lung biopsy. Can take sputum late in disease. Blood.
Stain:
Culture:
Identification:
Iodine-negative: Does not stain brown with iodine, as the inclusion bodies do not contain glycogen.
Serology: Indirect FA. Test for patient antibodies to the bugs, by using labelled anti-antibodies.
Acute-Convalescent titer of 4X
Treatment: Tetracycline.
MYCOPLASMA PNEUMONIA: No gram-stain.
Family Properties: MYCOPLASMACEAE
No Cell Wall: Only a triple-layer plasma membrane. Thus they are flexible, pliable, filterable.
Absolute Growth Requirements:
Cholesterol or other sterol for synthesis of plasma membrane.
Purines and pyrimidines.
Epidemiology / At Risk:
Ubiquitous. Normal flora of respiratory, GI, UG tract.
Infected spreads the organism for up to 14 weeks. Person-to-person spread of pneumonia occurs, and it tends to be found with close-living quarters, such as dorms, families, etc.
Manifestations:
Walking Pneumonia
Monocytic respose, lots of lymphocytes, which is normally found in a viral infection.
Infects ciliated cells in the bronchial region and multiples intracellularly. Thus it is ciliostatic, and it can make the cells lose their cilia altogether.
Other bug that infects same cells is B.Pertussis.
Non-productive or minimally productive cough.
WBC-count is not markedly high, maybe slightly high.
Otitis Media in adults. We can find bullous myringitis (inflammation of tympanic membrane).
Processing:
Specimen: Swab, sputum or ear aspirate.
Stain:
Culture: Biphasic Enriched Agar/Broth Medium. Agar with broth on top. 10 days.
They divide very slowly. Small fried-egg-like colony can be seen under scanning microscope after two weeks.
Absolute Growth Requirements:
Cholesterol or other sterol for synthesis of plasma membrane.
Purines and pyrimidines.
Identification:
Guinea-Pig RBC's: Add guinea-pig RBC's to the agar once the bugs have grown, and they should adhere to these cells (hemagglutination), making them easy to identify. In agar, hemolysis also occurs.
Cold-Agglutination Antibody Titration
Not sensitive, but still clinically useful.
PROCEDURE: An IgM antibody produced by the host cross-reacts with the I-antigen (type-O) blood-group antigen. Take the two and mix them together.
ANTIBODY: If found, it is the IgM antibody.
ANTIGEN: We use the type-O group-antigen.
If antibodies are present, hemagglutination will occur at 4C indicates a positive test. If the agglutination then dissolves when it is heated back up, then we have a positive test.
Test has theraputic applications: keep patient warm in order to prevent in-vivo hemagglut-ination with the bug.
Complement-Fixation Test: Specific test. Only useful if the test is positive. If antibody is present, then the lipid component of the bug's membrane will fix complement in the patient's serum.
Diagnostic antibody titer is 1:100, slightly high because it is an ubiquitous organism.
Virulence:
P1 Protein: Adhesin attaches to receptors on respiratory, GI, and UG tracts. It also gives the bug a characteristic gliding motility.
Host Immune Response: Monocytic.
Treatment: Tetracycline.
MYCOPLASMA HOMINIS: Emerging bug, associated with post-abortal and post-partum fevers, and PID.
UREAPLASMA UREALYTICA: Tiny bug.
Epidemiology / At Risk: Ubiquitous.
Manifestations: Urethritis which can be asymptomatic. Another causative agent of non-gonococcal urethritis.
Processing:
Culture: Very small colonies grow very slowly.
Identification: Add a pH indicator to medium to verify basic pH, which results from the presence of potent Urease.
Virulence: Urease helps bug survive in UG tract. Degrades urea and produces ammonia, yielding higher pH.
Treatment: Tetracycline.
RICKETTSIA RICKETTSIAE: Poorly staining gram-negative pleomorphic rods.
Family Properties: RICKETTSIACEAE
Strict Intracellular Parasites
Requirwe NAD and ATP for growth
OTHER SPECIES:
Ehrlichia: Arthropod-vectored infection of WBC's. No rash.
Coxiella: Q-Fever. Usually carried by farm animals.
RES involvement -- hepatosplenomegaly. Maybe no pneumonia.
No rash.
Epidemiology / At Risk: Found in the Eastern U.S., spread by ticks, in the Summer.
Manifestations: Rocky Mountain Spotted Fever is the best known example.
General Properties:
Arthropods are vectors.
They infect endothelial cells, starting with small capillaries and working their way up, leading to thrombosis and hemorrhage.
There is a prominent rash and fever.
Time Course:
4-7 days: Extensive rash, extending from extremities to trunk. Rash resembles Syphillus.
2 weeks: Very sick. High fever, DIC, hypotension, gram-negative shock.
Cardiac failure, renal failure, and encephalitis are likely causes of death.
OTHER RICKETTSIAL INFECTIONS:
Typhus: Several species and several vectors. Rash spreads from trunk to extremities, rather than RSMF which is the opposite.
Rickettsial Pox: From mites. Benign, self-limited rash.
Processing:
Specimen: Rash biopsy for RMSF.
Culture: Egg or tissue culture.
Identification:
Direct FA on endothelial cells
Serology: Indirect FA to measure antibody levels.
Antibody titer of 1:64, or Acute:Convelescent titer of 4X
Virulence:
Outer Membrane Proteins
Phospholipase: Acts as an invasin, helping bugs get into endothelial cells.
LPS: Strong endotoxic component.
Actin Polymerization: Making little projection to infect other cells. Some sort of way for the bugs to spread from cell to cell, similar to Shigella.
Host Immune Response: Probably combination of antibody plus cell-mediated. Not sure.
Vaccine / Prevention: Protective clothing.
Treatment: Tetracycline.
CHLAMYDIA TRACHOMATIS: Gram-negative rods.
Family Properties: CHLAMYDIACEAE
Obligate intracellular parasite
Tropic for columnar epithelia.
Gram-negative, but no peptidoglycan layer.
Dependent on ATP from host.
LIFE-CYCLE:
Elementary Body: Individual bugs living outside the host. They infect the host by endocytosis. They then multiply inside the host, utilizing host ATP.
Reticular Body: Cluster of bugs forming an inclusion body inside the cytoplasm of the host cell. They are released from the host-cell, to form more elementary bodies, which then go on to infect other cells.
Epidemiology / At Risk:
Leading cause of preventable blindness.
Leading cause of PID.
Manifestations:
Chronic Keratoconjunctivitis: Types A, B, C
Progressive conjunctivitis causes blindness by age 15 or 20.
Chlamydial Urethritis: Types D-K
So-called "Non-gonococcal urethritis."
PID
Inclusion Conjunctivitis (TRIC): Types D-K. Problem in newborns. Not the same as blindness above.
By law, (along with Gonococcus), newborns are treated prophylactically with eyedrops.
Lymphogranuloma Venereum: Types L1-L3.
Sexually transmitted, but the primary manifestation is suppurative (and later granulomatous) inflammation of inguinal lymph nodes.
Processing:
Specimen: Scrapings are taken for the inclusion conjunctivitis, UG, or rectal. Look for bugs in epithelial cells.
Stain: Giemsa stain. Iodine stain, looking for brown inclusion bodies.
Culture:
Identification:
Serotypes
A-C: Keratoconjunctivitris, found in Asia and Africa
D-K: Most prevelant in U.S. Urethritis and inclusion conjunctivitis.
L1-L3: Lymphogranuloma Venereum. Asia and Africa.
Iodine-Positive: Inclusion bodies contain a lot og glycogen and thus stain brown with iodine.
Virulence: Mostly focused on the Reticular Body.
ATPase: Helps the bug utilize the host cell's ATP.
ATP-ADP Translocase: In conjunction with the ATPase, this allows the bug to utilize the host cell ATP (high energy phosphate bonds) as a source of energy.
Cylindrical Projections: Little projections that probably help the bugs utilize host-cell nutrients.
LPS: Antigenic, providing a group-antigen for this bug.
Outer Membrane Proteins: Antigenic source for most of the serotyping (Types A-K, L1-L3).
Treatment: Tetracycline.
CHLAMYDIA PNEUMONIA: Gram-negative rods.
Manifestations: Walking Pneumonia, aka TWAR.
Infection of columnar epithelium of upper respiratory tract.
Identification: No processing usually needed. Disease can be treated based on clinical manifestation alone.
Treatment: Tetracycline.
CHLAMYDIA PSITTACI: Gram-negative rods.
Epidemiology / At Risk: Respiratory droplets inhaled. Found in pet birds (parrots, parakeets), poultry birds. People talking to their birds up close, etc.
Manifestations: Psitaccosis. An interstitial pneumonia.
Headache (can be severe), and dry, non-productive, hacking cough.
Sequelae: severe headache, encephalopathy, possible convulsions, coma, and death.
Processing:
Specimen: Lung biopsy. Can take sputum late in disease. Blood.
Stain:
Culture:
Identification:
Iodine-negative: Does not stain brown with iodine, as the inclusion bodies do not contain glycogen.
Serology: Indirect FA. Test for patient antibodies to the bugs, by using labelled anti-antibodies.
Acute-Convalescent titer of 4X
Treatment: Tetracycline.
MYCOPLASMA PNEUMONIA: No gram-stain.
Family Properties: MYCOPLASMACEAE
No Cell Wall: Only a triple-layer plasma membrane. Thus they are flexible, pliable, filterable.
Absolute Growth Requirements:
Cholesterol or other sterol for synthesis of plasma membrane.
Purines and pyrimidines.
Epidemiology / At Risk:
Ubiquitous. Normal flora of respiratory, GI, UG tract.
Infected spreads the organism for up to 14 weeks. Person-to-person spread of pneumonia occurs, and it tends to be found with close-living quarters, such as dorms, families, etc.
Manifestations:
Walking Pneumonia
Monocytic respose, lots of lymphocytes, which is normally found in a viral infection.
Infects ciliated cells in the bronchial region and multiples intracellularly. Thus it is ciliostatic, and it can make the cells lose their cilia altogether.
Other bug that infects same cells is B.Pertussis.
Non-productive or minimally productive cough.
WBC-count is not markedly high, maybe slightly high.
Otitis Media in adults. We can find bullous myringitis (inflammation of tympanic membrane).
Processing:
Specimen: Swab, sputum or ear aspirate.
Stain:
Culture: Biphasic Enriched Agar/Broth Medium. Agar with broth on top. 10 days.
They divide very slowly. Small fried-egg-like colony can be seen under scanning microscope after two weeks.
Absolute Growth Requirements:
Cholesterol or other sterol for synthesis of plasma membrane.
Purines and pyrimidines.
Identification:
Guinea-Pig RBC's: Add guinea-pig RBC's to the agar once the bugs have grown, and they should adhere to these cells (hemagglutination), making them easy to identify. In agar, hemolysis also occurs.
Cold-Agglutination Antibody Titration
Not sensitive, but still clinically useful.
PROCEDURE: An IgM antibody produced by the host cross-reacts with the I-antigen (type-O) blood-group antigen. Take the two and mix them together.
ANTIBODY: If found, it is the IgM antibody.
ANTIGEN: We use the type-O group-antigen.
If antibodies are present, hemagglutination will occur at 4C indicates a positive test. If the agglutination then dissolves when it is heated back up, then we have a positive test.
Test has theraputic applications: keep patient warm in order to prevent in-vivo hemagglut-ination with the bug.
Complement-Fixation Test: Specific test. Only useful if the test is positive. If antibody is present, then the lipid component of the bug's membrane will fix complement in the patient's serum.
Diagnostic antibody titer is 1:100, slightly high because it is an ubiquitous organism.
Virulence:
P1 Protein: Adhesin attaches to receptors on respiratory, GI, and UG tracts. It also gives the bug a characteristic gliding motility.
Host Immune Response: Monocytic.
Treatment: Tetracycline.
MYCOPLASMA HOMINIS: Emerging bug, associated with post-abortal and post-partum fevers, and PID.
UREAPLASMA UREALYTICA: Tiny bug.
Epidemiology / At Risk: Ubiquitous.
Manifestations: Urethritis which can be asymptomatic. Another causative agent of non-gonococcal urethritis.
Processing:
Culture: Very small colonies grow very slowly.
Identification: Add a pH indicator to medium to verify basic pH, which results from the presence of potent Urease.
Virulence: Urease helps bug survive in UG tract. Degrades urea and produces ammonia, yielding higher pH.
Treatment: Tetracycline.