L25- RTI IX Flashcards
Ornithosis, formerly called (1), is caused by (2) which is a (3) type microbe of (4) size.
1- psittacosis, parrot fever
2- chlamydophila psittaci
3- parasite of eukaryotic cells
4- 0.45 µm
Chlamyodophila psittaci:
- (1) location during infection
- Gram(+/-)
- (3) are the reservoirs
- (4) are the forms
1- obligate intracellular
2- gram- (not staining wise, but yes structurally)
3- birds
4- EB (infectious), RB (replicative) forms
Chlamyodophila psittaci:
- outer cell wall resembles (1) and contains (2), but lacks (3)
- its shape is considered (4)
- (5) is the major component of the outer cell wall is common and unique to each chlamydia species
1- gram- 2- weakly endotoxic LPS 3- peptidoglycan 4- round with thin periplasmic space 5- MOMP- major outer membrane protein
briefly describe the life cycle of chlamyodophila psittaci
1) EB attaches to target cell (via microvilli)
2) EB endocytosis and prevents fusion with lysosome
3) EB –> RB
4) RB replication via binary fission
5) RB –> EB (inclusion bodies contain both)
6) lysis of cells and inclusion bodies for release of virus
in chlamyodophila psittaci life cycle, it takes (1) time for EBs to penetrate and becomes active RB and then takes (2) amount of time to reform EBs
1- 6-8 hrs post-penetration (EB –> RBs)
2- 18-24 hrs later (RB –> EB)
Clamyodophila psittaci:
- (1) is the method of transmission
- spreads to (2) parts of liver, kidneys to cause (3)
-(4) list the many respiratory effects
1- urine or respiratory droplets of birds
2- reticuloendothelial system
3- necrosis
4:
- lymphacytic inflammation of alveoli
- edema, thickening of alveolar wall
- infiltration of macrophages, necrosis and occasional hemorrhages
- mucus plugs bronchioles –> cyanosis, anoxia
what are the high risk factors associates with ornithosis
(bird exposure)
- vets, zookeepers
- pet shop owners
- employees of poultry processing plants
Ornithosis / chlamydophila psittaci:
- (1) incubation period
- (2) initial sxs
- (3) pulmonary sxs
- (4) CNS sxs
- (5) GI sxs
- (6) other possible developments
1- 5-14 days
2- HA, high fever, chills, myalgia
3- nonproductive cough, consolidation
4- (common) encephalitis, convulsions, coma, death
5- n/v/d
6- hepatosplenomegaly, follicular keratoconjunctivitis
Ornithosis:
- (1) Dx
- (2) Tx
- (3) additional prevention strategies
1- serology (maybe PCR)
2- antibiotics + patient isolation
3- (no vaccines available) antibiotic treatment for infected birds
HPS, aka (1), is commonly associated with (2) vector. It is characterized by (3) symptoms leading into (4) symptoms, and then finally (5).
1- hantavirus pulmonary syndrome 2- rodent 3- febrile prodrome 4- acute respiratory failure 5- death due to circulatory collapse
HPS is caused by viruses in the (1) family, (2) virus is most common. Most cases in the US happen in (3) region.
1- bunyaviridae family (hantavirus)
2- sin nombre virus
3- west of the Mississippi River (>96% of cases)
Bunyaviridae / SNV are (non-/enveloped) (+/-) (ss/ds) (RNA/DNA) with a (5) shape
(sin nombre virus)
enveloped (lipids + 2 major glycoproteins) (-) sense ssRNA, spherical
(1) is the main risk factor for HPS, and usually affects people in (2) areas, where (3) are potential sites.
Hantaviruses can also cause (4) in addition to HPS.
1- rodent infestation
2- rural areas
3- peridomestic sites: barns, outbuildings, sheds
4- HFRS- hemorrhagic fever with renal syndrome
SNV is transmitted via (1), primarily in (2) season.
(sin nombre virus)
1- airborne transmission in rodent droppings (urine, feces, saliva)
2- fall
HPS clinical features:
- (1) incubation period
- (2) 1st phase
- (3) 2nd phase
- (4) 3rd phase
- (5) mortality rate
1- 1-8 wks
2- Prodromal (3-5 days): viral illness of fever, HA, myalgia, v/d (similar to viral gastroenteritis)
3- Cardiopulmonary (24-48hrs): dyspnea, dry cough, pulmonary edema, circulatory collapse
4- Convalescent: significant diuresis, sxs improve and complete recovery over wks
5- 50% fatality rate
HPS:
- (1) increases in blood vessels due to (2) as a consequence of (3) response
- (1) leads to (4) directly
- onset of symptoms is dependent on (5) and organs affected depends on (6)
1- inc capillary permeability 2- endothelial damage 3- immunological response to viral Ags that penetrated endothelium 4- widespread protein rich edema 5- specific Igs for virus 6- specific species of Hantavirus
describe the diagnosis and treatment of HPS
-initial phase is often missed, Rodent Exposure is most critical
Dx: RT-PCR (viral RNA), ELISA for IgM/G against Hantavirus
Tx: supportive, no specific Txs available
Melioidosis, aka (1), is caused by (2) microbe in (3) geographic areas and in (4) parts of the environment.
1- Whitemore’s disease
2- Burkholderia pseudomallei
3- (endemic regions) South Asia, SE Asia (+ China), northern Australia
4- soil, fresh water (therefore common in the rainy season)
Burkholderia pseudomallei causes (1). It is a Gram(+/-) (non-/motile) (aerobe/anaerobe) (extra/intra)-cellular (non-/spore forming) (coccus/bacillus).
1- Melioidosis
2- Gram-, non-motile, aerobe, facultative intracellular, non-spore forming bacilli
describe the transmission of Burkholderia pseudomallei
- *percutaneous inoculation, *inhalation, aspiration, ingestion (occasionally)
- mainly thru broken skin, inoculation during exposure to wet soils, contaminated water
- rarely ever person to person, animal exposure, sexual transmission
Meliodosis clinical features:
- most cases present as (1)
- (2) are the risk factors for symptom development
- (3) are the most common clinical manifestations
1- asymptomatic, 90%
2- DM, excess EtOH, CRD, chronic lung disease, CF, thalassemia
3- pneumonia, localized skin infection (acute or chronic or latent- like in Tb)
Meliodosis is mostly seen in (adults/children) and presents as (2) in contrast to (adult/children) which present with (4) instead.
1- adults
2- pneumonia
3- children
4- cutaneous infections (ulcer, abscess)
Meliodosis is caused by (1). (2- indicate the best one) samples can be taken for culture. (1) is cultured on a (3) agar and (4) is the hallmark feature.
1- berkholderia pseudomallei
2- *sputum, blood, urine, abscess fluid, swab from skin/throat/rectal
3- Ashdown’s agar (selective media)- note it also has bipolar staining
4- cauliflower head appearance
describe the prevention of meliodosis
(berkholderia pseudomallei- no vaccine)
-avoid contact with soil, standing water in endemic regions
-boots, gloves during agricultural work
Q fever is caused by (1), usually found in (2) and transmission occurs via (3).
1- coxiella burnetti
2- cattle, sheep, goats (ticks)
3- inhalation of aerolized particles (other methods exist too)
Coxiella burnetii causes (1). It is a gram(+/-) (extra/intra)-cellular (4) type microbe.
1- Q fever
2- gram-
3- obligate intracellular
4- parasite
Q fever caused by (1), has an incubation period of (2). Normally infections will present as (3). Other manifestations of a Q fever include (4), (5), (6).
1- coxiella burnetti 2- 3-4 weeks 3- asymptomatic 4- self limiting flu like illness 5- pneumonia (N. America) 6- hepatitis (Europe)
describe the phases of Coxiella burnetti infections and include what determine the infectious status
-infections are dependent on LPS status (intact or truncated)
Phase I- highly infectious, intact LPS
Phase II- (in vitro) not infectious, truncated LPS
Q fever clinical presentation:
- (1) common symptoms
- (2) complicated / chronic symptoms
- (3) is a complication that can occur years after primary infection, usually due to one of (4) risk factors
1- fever, HA, chills, rash (20%), pneumonia or hepatitis (depending on type)
2- osteomyelitis, encephalitis, endocarditis
3- culture negative endocarditis
4- pre-existing heart defects, pregnancy, immunocompromised
Q fever:
- (1) cause
- (2) Dx
- (3) Tx
1- coxiella burnetti
2- serology (phase I, II): IgM peaks at 4-6 wks
3- doxycycline +/- surgery for endocarditis
