Microbiology Flashcards
1
Q
reportable condition
A
every case of disease must be reported at the state level
2
Q
notifiable condition
A
data must be forwarded to the CDC→morbidity and mortality weekly report and annual report
3
Q
SARS 2003
A
- new highly contagious pneumonia
- started in China
- animal (civet) coronavirus
- 8,000 cases, 800 deaths
4
Q
Swine Flu 2009
A
- H1N1 virus
- started in Mexico
- triple recombination between human and animal influenza virus
- not nearly as bad as 1918 or 1968 pandemics
- 250,000 deaths
5
Q
MERS 2013-2014
A
- started in Saudi Arabia
- coronavirus endemic to camels, appeared in humans in 2011
- 100 deaths
6
Q
Ebola 2014-2015
A
- sudden resurgence of mutated bat virus
- hemorrhagic fever
- 27,000 cases, 11,000 deaths
7
Q
general trends of infectious disease
A
- continuing reductions of vaccine-preventable infections
- gradual increase in pertussis, legionella, and syphilis
- occasional outbreaks of previously known conditions and occasional emergence of previously unknown microorganism
8
Q
N. gonorrhoeae
A
- gram- diplococci (kidney bean shaped); facultative aerobe; oxidase+; catalase+
- women usually asymptomatic
- neonates must be protected by prophylatic eye ointement (prevents opthalmia and blindness)
- virulence factors: IgA proteases, pili, LOS, porins, Opa
- testing: NAAT preferred but culture may be required for sensitivity testing
- use thayer-martin if normal flora, use chocolate if normally sterile
- treatment: ceftriaxone
9
Q
C. trachomatis
A
- small obligate intracellular bacterium
- elementary bodies (tiny infectious rugged cells) “unpack” into reticulate bodies after infection, form inclusions and replicate
- 18 serovars
- testing: NAAT preferred but cuture works well (does not gram stain though)
- test for coincidence chlamydia in all STD patients
- treatment: doxycycline (erythromycin for pregnant/ pediatric/ allergic patients)
10
Q
what are the 18 serovars of c. trachomatis?
A
- A, B, Ba, C: blinding trachoma (leading cause of preventable blindness in Africa)
- L1-L3: lymphogranuloma venereum ( small, painless ulcer→swollen painful lymph nodes)
- D-K: genital tract infection (MC bacterial STD in US; men often asymptomatic; possibility for verticle transmission)
- pneumonia
11
Q
pediculosis
A
- head lice: school kids, itchy behind ears
- body lice: homeless, itchy at night
-
pubic lice (crabs): promiscuous individuals, itchy groin
- perform full STD panel as well
- visual diagnosis
- treatment: nit combing and hot laundering
12
Q
spirochetes
A
- spiral shaped with axial filament→corkscrew motion
- too small to see by microscopy, can’t be cultured, and poorly visible on gram stain (gram- envelope) so use darkfield
13
Q
T. pallidum
A
- extremely infectious obligate pathogen (not intracellular)
- invade lymphatics and blood stream immediately and virulence is based on immune evasion→low inflammation and humans rise mostly-usely antibodies (reagin)
- labs: serology for reagin (VDRL, RPR) is best test for disease-in-progress, confirm exposure with tests for treponeme-specific antibodies
- treatment: single injection of penicillin G
- potential for Jarisch-Herxheimer reaction
14
Q
what are the stages of syphilis?
A
- primary: 3-6 weeks→ painless chancre at site of infection
- secondary: 4-10 weeks→body-wide rashes, condylomata lata, patchy alopecia
- latent: organism remains although secondary symptoms resolve
-
tertiary: 3-10 years later→ gummas, neurosyphilis (meningitis, tabes dorsalis, general paresis)
- check for argyll-robertson pupil
- cardiac involvement
- congenital syphilis: kills 50% fetus/newborn, survivors are infected→ bone deformities, interstitial keratitis
15
Q
Yaws and Pinta
A
- both are treponema infections (like syphilis) but are transmitted through direct contact
- both will give +VDRL and +RPR
- yaws: primarily a dermatologic manifestation
- pinta: hypo and hyperpigmented skin plaques
16
Q
common features of oncogenes
A
- makes tumors if transplanted to animals
- undifferentiated
- immortal
- not contact inhibited
- resistant to apoptosis
- abnormal chromosomes
17
Q
list 7 protooncogenes
A
- Myc: transcription factor
- Src: membran signaling growth factor binding
- Ras: signal transduction from surface receptors
- Sis: platelet derived growth factor
- Erb B: growth factor receptor
- Fms: growth factor receptor
- LMO2: hematopoiesis
18
Q
tumor suppressors
A
- control cell cycle
- inactivation (e.g., of p53 or Rb)→ cell proliferation and accumulation of other mutations
19
Q
RNA oncoviruses
A
- cause cancer in animals by transmission of activated oncogenes or by insertional activation of an oncogene
- e.g., human T-cell leukemia virus
20
Q
DNA oncoviruses
A
- cause cancer through effects of T antigen or its equivalent which target p53 and Rb genes
- e.g, HPV, HHV8, Hep B, Epstein Barr
21
Q
papillomaviruses
A
- low risk→warts
- intermediate risk→laryngeal papillomas
- high risk→cervical, pharyngeal cancer
- loss of E2 function because of integration of HPV to host cell genome allows over-expression of E6 and E7
- E6 binds p53 and leads to degradation by ubiquitin pathway
- E7 binds Rb and prevents its interaction with E2F
22
Q
Epstein Barr virus
A
- causes mono but can transform human B cells (translocation puts myc gene under control of immunoglobulin promoter)
- Burkitt’s lymphoma: endemic in Africa, tumor of prepubertal boys
- Nasopharyngeal cancer: endemic in Asian and Arctic; IgA antibodies to EBV capsid antigen predict tumors or recurrences
- can be seen in patients who are immunocompromised
23
Q
Hep B
A
- no consistent expression of viral protein in cancer cells; no activation of cellular oncogene
- virus x gene plus ras can transform liver cells in culture
24
Q
Kaposi’s sarcoma
A
- herpesvirus (HHV8)
- AIDS defining illness
25
Q
human T cell leukemia virus
A
retrovirus that causes T cell leukemias/lymphomas
26
Q
describe the history and current epidemiology of AIDS
A
- first reported June 1981 in LA
- 40-45,000 new cases of HIV/year
- males outnumber females 4:1; 4/5 of male infection is from male to male sexual contact vs. majority of infection is in heterosexual relations for women
- HAART 1986: diagnosis of AIDS and death rate dropped
27
Q
how do we define AIDS?
A
CD4 count < 200 OR HIV + AIDS defining illness
28
Q
what are the CD4 counts for common AIDS-related conditions?
A
- 500: skin disease
- 350: pulmonary TB
- 200: kaposi sarcoma
29
Q
goals of AIDS treatment
A
- suppress HIV-1 replication (which also prevents spread of HIV)
- prevent/delay destruction of immune system
- achieve normal survival while mainaining a tolerable life
30
Q
HAART
A
- highly active antiretroviral therapy
- treat whether patients are/aren’t symptomatic
- asymptomatic treatment used to be based on CD4 counts and viral loads
- consider deferral of ART if clinical or personal factors support deferral, if there are significant barriers to adherence, if comorbidies complicate or prohibit ART or if patients are elite controllers (long term non-progressors)
31
Q
AZT
A
historically used to treat AIDS, had initial benefit then rebounding of disease due to acquired resistance
32
Q
HIV replication
A
- attachment/ fusion
- uncoating
- RT of ssDNA to DNA
- circular genome→ nucleus
- genome integration and latency
- HIV mRNA made by host RNApolII
- lytic replication, protease cuts proteins during sorting
- virion budding and maturation (not infectious)
- trapezoidal capsule formed by protease mediated conformational change
33
Q
mechanism of HIV disease
A
infects lymphoid cels in vaginal/rectal epithelium→ lymphoid organs → establishment of chronic infection→ immune activation by cytokines and Env-mediated aberrant cell singaling→ accelerated virus replication→ destruction of immune system
- Env mediates virion attachment and entry into T cell and macrophages
- Env can fuse T cells with uninfected T cells→ syncytia
- abnormal cytokine response to Env
- hyperactivation of B cells but not T cells prevents mature Ig response
