Micro Test 3A Flashcards

1
Q

Haemopholus influenza

A
Main Biological Features
-gram negative, encapsulated rod
-fastidiuous and sensitive to drying, temp. extremes, and disinfectants
- normal colonist of respiratory tract and vagina
-facultative anaerobe
Clinical manifestations
-bacterial meningitis(high death rate)
-epiglottis, otitis media, sinusitis, pneumonia, and bronchitis
-conjuctivitis (pink eye)
Mechanism of Disease
-LPS, capules
Transmission
-respiratory droplets
-aerosols
Prevention
-vaccines
-better diagnosis
Treatment
-cephalosporin, antibiotics
-
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2
Q

Spirochetes

A

Main Biological Features

  • gram neg. human pathogens
  • free living saprobes, or commensals of animals, not primary pathogens
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3
Q

Genus Treponema(spirochetes)

A

Main biological features

  • thin, coiled cells
  • live in oral cavity, intestinal tract, and perigenital regions of humans and animals
  • pathogens
  • strict parasites
  • need live cells for cultivation
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4
Q

Treponema Pallidum

A

Main biological features
- thin, gram -, spirochetes, strict parasites
- fastidious and sensitive to environment
Clinical Manifestations
- syphillis (3 stages separated by latency, primary(formation of chancre)moves into blood stream for latency, secondary(weeks to months later, fever, headache, sore throat, rash) multiplied in blood, tertiary(yrs. later swollen gums(gummas) neural and cardiovascular problems.(Dementia)
- Congential syphillis (bone deformation, nervous system abnormal, skin eruptions, nasal discharge)
Mechanisms of Disease
-hooked tip for binding to epithelial cells, outer membrane protein inducing inflammation and tissue damage
Transmission
- std and transplacental
Prevention
- no vaccine, prophylactic pennicillin, high risk identification
Treatment
-penicillin G

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5
Q

Nonsyphilitic Treponematoses

  • Leptospira
  • Leptospirosis
A

Main Biological Features
-tight, coils bend/hook at one or both ends

L. biflexa
- harmless, free- living sap robe
L. interrogans
-causes leptospirosis, a zoonosis
-bacteria shed in urine
- infection from contact w/ urine, targets kidneys, liver, brain, eyes
- sudden high fever, chills, headache, muscle aches, conjuctivitis, + vomiting
- long term infections may affect kidneys and liver
- 50-60 cases a year

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6
Q

Genus Borrelia

A
  • large spirochetes 3-10 coils irregularly spaced

- transmitted by arthropod vector

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7
Q

B. burgdorferi (lyme disease)

A

Main Biological Features
- large spirochetes, coils irregularly spaced
- arthropod vector
-tick/ deer lifecycle, larval tick to mouse, tick develops jumps to human or deer, lay eggs start cycle again
Clinical Manifestations
-lyme disease, non fatal, bulls eye lesion, rheumatoid and neuromuscular function
Mechanisms of Disease
-hook that binds to epithelial cells at ends
Transmission
- hard ticks(black legged deer tick)
Prevention
-removal, preventative antibiotics
- vaccines for high risk and dogs
Treatment
- antibiotics

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8
Q

Curviform Bacteria

A
  • gram negative
    -generally enteric diseases
    vibrio- single polar flagellum, comma shaped rod
    campylobacter- short spirals/ curved rods, one flagellum
    heliobacter- spirochete w/ tight spirals + several polar flagellum
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9
Q

Vibro Cholera

A
Main biological features
-gram negative
- single polar flagellum
-comma shaped rods
-El Tor biotype- survives longer, more infectious
-fermentive
Clinical Manifestations
- diarrhea equals severe dehydration leading to muscle, circulatory, and neurological symptoms
Mechanisms of Disease
- cholera toxin- causes electrolyte and water loss "rice water stool"
Transmission
-bacteria is ingested in food or water
Prevention
-proper food sanitation
Treatment
- antibiotics and rehydration
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10
Q

Vibrio parahaemolyticus

Vibrio vulnificus

A

Salt tolerant inhabitants of coastal waters
VP- gastroenteritis from raw seafood, symptoms similar to cholera
VV- gastroenteritis from raw oysters, serous complications in persons with diabetes or liver disease
Treatment fluid plus electrolyte replacement, occasionally antimicrobials

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11
Q

Campylobacter jejuni

A
Main biological features
-small curved gram- rods
-bacilli
-polar flagella
-microaerophillic
-oxidase positive
-nonfermenting
Clinical manifestations
-gastroenteritis (fever, diarrhea, abdominal pain)
Mechanisms of Disease
- CJT- a heatlabile enterotoxin that stimulates secretory diarrhea
Transmission
-contaminated food, water, milk, meat, chicken, and beverages
Prevention
-proper food harvesting and preparation
Treatment
-self limiting
-antibiotics, rehydration
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12
Q

Chlamydia trachomatis

A

Main biological features
-very small, gram neg. pleomorphic rods
-obligate intracellular parasite
-elementary body- small metabolic inactive, infectious formed by infectious host
-reticulate body- noninfectious, actively dividing within host cell vacuoles
-invades epithelial and lymphatic cells
Clinical Manifestations
-chlamydiosis, urethritis, pelvic inflammatory disease, and -lymphogranuloma venerum(lymphatic obstruction causing painful deformation) in genitalia/ pelvic lymphatics
-trachoma- attacks mucuous membrane of eyes, lungs, genitourinary tract
-ocular trachoma, inclusion conjunctivitis
Mechanisms of Disease
-cell wall inhibits phagolysosome fusion allowing reticulate bodies to survive and multiply in phagosomes
-elementary bodies encased in impervious envelope insuring survival outside host cell
Transmission
-std
-secretions
Prevention
-condoms
-newborn prophylaxis
Treatment
-antibiotics

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13
Q

Chlamydophila

A

-members used to be members of genus Chlymadia
-C. pneumoniae- causes atypical pneumonia that is serious in asthma patients
C. psittaci- causes ornithosis, zoonosis through birds, pneumonia/flulike infection w/ fever, lung congestion

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14
Q

Viruse features

A
  • noncellular particles with the definite size, shape, and chemical composition
  • most abundant microbes on earth
  • played a role on the evolution of bacteria, archaea, eukarya
  • Obligate intracellular parasites
  • lack protein synthesizing machinery
  • Only contain parts needed to invade and control host cell
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15
Q

Virus structure

A

-protein capsids
-nucleic acids and capsid make nucleocapsid
-some viruses have an envelope, those lacking an envelope are naked
-Capsomers are identical proteins subunits (form capsid)
Two capsid structures
Helical, icosahedral
Viral envelope
-Mostly animal viruses
-Acquired when the virus leaves the host cell
-Exposed proteins on outside of the envelope called spikes are essential for attaching

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16
Q

Complex viruses

A
  • Poxvirus lacks a typical capsid and are covered by a dense layer of lipoproteins
  • Some bacteriaphages have a polyhedral nucleocapsid along with a helical tail and attachment fibers
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17
Q

DNA viruses

A
  • double-stranded but maybe single-stranded

- Circular or linear

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18
Q

RNA Viruses

A

Single stranded, double-stranded, maybe segmented into separate RNA pieces

  • positive sense RNA is ready for immediate translation
  • Negative sense RNA genome must be converted into proper form(need RNA polymerase to make into a positive strand
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19
Q

General phases in an animal virus multiplication cycle

A
  • adsorption-binding the virus to specific molecules on the host cell
  • penetration- genome enters the host cell, endocytosis or fusion
  • uncoating- release of genetic material from capsid,
  • Synthesis- viral components are produced
  • Assembly- new viral particles are constructed
  • Release-viruses released by budding(exocytosis) or cell lysis
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20
Q

virus info (acute/persistent)

A

acute- infection only has lytic cycle
persistent- lytic and lysogenic
chronic- lytic and lysogenic at same time(always fatal)
episomal positioning- virus hides in nucleus/ cytoplasm

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21
Q

Multiplication cycle in bacteriophages(bacterial viruses)

A

adsorption- virus binds to specific host molecules
penetration- genome enters host cell
replication- viral components are produced
assembly- viral components are assembled
maturation- completion of viral formation
lysis/release- virus leaves cell to infect other cells

22
Q

temperate phages

A
  • don’t replicate, just adsorption and penetration
23
Q

lysogeny

A

prophage retained and copied during normal cell division, spread without cell death

  • corynbacterium diphtheriae
  • vibrio cholerae
  • clostridium botulinum
24
Q

Prions

A
  • Miss folded proteins, Contain no nucleic acid, always fatal, don’t denature even if cooked
  • No vaccine, no cure, no treatment
  • cause transmissable spongiform encephalopathies(fatal neurodegenerative disease)
  • scrapie- in sheep and goats
  • BSE(mad cow disease)
  • wasting disease in elk
  • humans- Creutzfeldt-Jakob Syndrome(CJS)
25
Q

Satellite viruses

A
  • depended on other viruses for replication
  • adeno-associated virus- replicates only in cells affected with adenovirus
  • delta agent- naked strand of RNA expressed only in the presence of Hep B
  • virioids- short pieces of RNA, no protein coat in plants
26
Q

DNA vs. RNA viruses

A
  • DNA- double standards except for parvovirus, budded off nucleus
  • RNA-Single stranded except for Reoviruses, multiply and release in cytoplasm
27
Q

chronic infection

latent infection

A
  • chronic- detectable, multiply at slow rate, mild/absent symptoms
  • latent- after lytic cycle, dormant, undetectable, can reactivate
28
Q

oncogenic

teratogenic

A
  • cancer causing

- development disturbances and defects from crossing placenta

29
Q

Poxvirus(small pox)

A
Main biological features
-DNA virus
-largest genome of viruses
-1st eliminated by vaccination
Clinical manifestations
-pox- skin pustules
- fever, malaise, rash
-variola major- high virulence, toxemia, shock, intravascular coagulation(30% mortality)
-variola minor- less virulent, mostly skin
Mechanism of disease
-envelope
Transmission
-exposure through skin, skin contact
-potential germ warfare
-inhalation, droplets
Prevention
-vaccine
Treatment
-self immunization
30
Q

Molluscum Contagiosum virus

A
  • in U.S. an std
  • DNA poxvirus
  • small benign lumps(smooth elevated lesions), in genital/thigh area
  • treatment freezing, cautery
  • transmit through fomites
  • primarily in children
31
Q

Herpes simplex virus 1 and 2

A

Main biological features
-virus with that icosahedral capsid
-DNA virus
Clinical manifestations
-HSV-1-lesions on the oropharynx(herpes labials), encephalitis, herpetic gingivomatitis(in mouth), herptic keratitis(eye)
-HSV-2-lesions on the genitalia, (genital herpes)
-herpetic Whitlow(both) are deep painful vesicles caused when virus enters a cut in the skin
Mechanism of disease
-Latency with entry of the HSV episome into the nucleus of the neurons
-HSV-1- enters 5th cranial nerve
-HSV-2- enters lumbosacral nerve trunk ganglia
Transmission
-exposure to secretions
-Active lesions most significant source
Prevention
-Screen pregnant women
-safe sex practices
-avoiding active lesions during lytic cycle
Treatment
-antibiotics prevent lytic cycle
-oral medication for genital herpes
-topical medications

32
Q

Varicella-Zoster Virus

A
Main biological features
-Envelope virus with an icosahedral capsid
-Enters and remains latent in neurons
-DNA virus
Clinical manifestations
-varicella(chickenpox)
-zoster(shingles)
Mechanism of disease
-Latency in ganglia
Transmission
-respiratory droplets
Prevention
-Chickenpox vaccine
-Shingles vaccine
Treatment
-Alleviation of discomfort
-prevention of secondary bacterial infections
33
Q

Cytomegalovirus Group

A

Main biological features

  • DNA virus
  • produce giant cells with nuclear and cytoplasmic inclusions
  • Leading causes of infectious congenital abnormalities
  • Transmitted in saliva, respiratory mucus, breast milk, urine, semen, cervical secretions
  • Uses own DNA polymerase
  • chiefly invades immuno suppressed
34
Q

Epstein-Barr virus

A

Main biological features
-envelope virus with an icosahedral capsid
-DNA virus
-infects B-lymphocytes (white blood cells that make antibodies)
-90-95% pop. are infected
Clinical manifestations
-infectious mononucleosis(mono, kissing)
-Burkitt lymphoma-cell becomes cancer cell through integration of DNA( swollen jaw) responds well to treatment
-nasopharyngeal carcinoma-cancer throat/nose epithelial cells
Mechanism of disease
-latency, ability to Incorporate DNA into that of the host
Transmission
-direct, oral contact, and contamination of saliva
Prevention
-no vaccine, Avoid contact
Treatment
-alleviation symptoms
-antivirals for severe mono
-chemotherapy for Burkitt

35
Q

Human herpes virus 6, human B-lymphotropic virus

A

Clinical Manifestations
-DNA virus
-mono like symptoms, lymphadenopathy and hepatitis
-roseola caused by HH6/7
-significant relationship btwn HHV-6 and Hodgkins lymphoma, oral carcinoma, and T-cell leukemias
-Kaposi’s sarcoma-associate virus or HHV-8 is linked with common tumors of AIDS
Transmission
-infects bcells through saliva

36
Q

Hepatitis B virus
(hepatitis- an inflammatory disease of liver cells that may result from several viruses, Hep B(DNA), Hep a(RNA), Hep c(RNA)

A

Main biological features
- small enveloped virus
-DNA virus
-can perform reverse transcriptase
Clinical manifestations
-most people show no symptoms and development immunity to the virus
-malaise, fever, discomfort, rashes, arthritis, jaundice
-can become a chronic infection
-increase risk of liver cancer, hepatocellular carcinoma
-small # develop chronic liver disease(necrosis/cirrhosis)
Mechanism of disease
-persistence in liver cells, and integration into the genome, Leading to oncogenesis
Transmission
-Break in skin or mucous membrane or by injection
Prevention
-vaccine(produced completely by genetic engineering)
-Passive immunization with HBIG for persons exposed and neonates
Treatment
-mild infections just manage symptoms
-passive immunization(above)

37
Q

Human Papillomavirus

A

Main biological features
-small, non-enveloped DNA virus
-Circular DNA
-Causes persistent infections and tumors
-HPV16/18 90% cervical cancers
Clinical manifestations
-papilloma(2-5yr incubation)-Squamous epithelial growth, wart, or verruca
-common seed warts-painless, elevated rough growth on fingers
-plantar warts- deep, painful, on soles of feet
-genital warts- most common STD in U.S.
Mechanism of disease
-ability to persistent epithelial cells of the genitalia
-can insert in genome and cause oncogenesis
-can inhibit P53 which allow cell death
Transmission
-Direct contact
Prevention
-Barrier protection
-vaccine, prevents strains most closely linked to cancer
Treatment
-early detection, women pap smear
-removal of the wart
Chemically, With surgery, freezing, or with cauterization, warts can return

38
Q

Influenza virus

A

Main biological features
-Envelope, spherical virus
-segmenting genome of seven or eight strands of single stranded RNA
-three antivirus types, A, B, C, type a causes most infections
-grows well at core temp. 37C
Clinical manifestations
-influenza B-seasonal flu(antigenic drift)
-Influenza C-minor respiratory disease, involved in epidemics
-Influenza acute respiratory illness, seasonal pandemics, severe respiratory inflammation, fever, headache, pharyngeal pain, shortness of breath, coughing
Mechanisms of disease
-hemagglutinin and neuraminidase spikes
-can undergo antigenic shift(virus changes) and antigenic drift(becomes less susceptible to antiviral)
Transmission
-inhalation of aerosols and droplets
-fomites
Prevention
-seasonal vaccine
Treatment
-neuriminidase inhibitor(prevents budding and release)
-anti inflammatories, pain relievers to help symptoms

39
Q

Parainfluenza

A
  • RNA virus
  • widespread as influenza but more benign
  • respiratory transmission
  • most in children
  • minor cold, bronchitis, croup
  • no treatment
40
Q

Mumps(epidemic parotitis, self limited swelling of parotid salivary glands)

A

Main biological features

  • RNA virus
  • humans only reservoir
  • one time infection creates lifelong immunity
  • 2 To three weeks of fever, muscle pain, classic swelling one or both cheeks
  • Usually uncomplicated can’t make males and females sterile
  • MMR vaccine
  • Symptomatic treatment
41
Q

Measles(caused by Morbillivirus)(red measles/rubeola)

A

Main biological features
-envelope virus
-Not segmented single-strand RNA genome
-Humans are the only reservoir
Clinical manifestations
-measles(rubeola)- sore throat, dry cough,, fever, Oral lesions called Koplik’s spots,
-exanthem-maculopapular rash over most of the body
-panencephalitis, Progressive neurological disease resulting in coma and death
-Secondary bacterial infections
Mechanism of disease
-synctium formation
Transmission
-one of the most contagious infectious diseases, transmitted by respiratory aerosols
-Humans on the reservoir
Prevention
-MMR vaccine
Treatment
-reduce fever, suppress cough, replace lost fluids
-high mortality worldwide, Low in the US

42
Q

Pneumovirus(Respiratory Synctial Virus)

A

-RNA virus
-infects upper respiratory tract increases giant
multinucleated cells(synctium)
-most prevalent cause of respiratory infection and children six months or younger
Transmission
-epithelia of nose and eye
Treatment
-a monoclonal antibody that blocks attachment

43
Q

Rabies

A
Main biological features
-rhabdovirus
-Enveloped, bullet shaped virions
-slow, progressive zoonotic disease
-RNA virus
Clinical manifestations
-Rabies, clinical phases
-prodromal phase-Fever, nausea, vomiting, headache, fatigue, burning, tingling sensation a wound site
-Furious phase-Agitation, disorientation, seizures, twitching, hydrophobia
-Dumb phase-paralyzed, disoriented, stuporous
-, Face-Results and death
Mechanism of disease
-negri bodies- intracellular inclusions in nervous tissue
-envelope
Transmission
-bite from wild or stray animals
Prevention
-don't get bit
-rabies vaccination
-Vaccine works before or after
-vaccination of domestic animals
Treatment
-Six dose and two booster vaccine
44
Q

Rubella(teratogenic)

A

Main biological features
-caused by Rubivirus, a Togavirus
-Single stranded RNA with a loose envelope
German measles
Endemic disease
Clinical manifestations
-Postnatal infection-fever, sore throat, rash, three days
-Congenital infection-infect during first trimester induces miscarriage or defects
Transmission
Transmitted through contact with respiratory secretions
Treatment
No specific treatment
Prevention
Attenuated viral vaccine MMR

45
Q

Hepatitis C virus (HCV)

A
RNA virus
Transmission
-Blood transfusions, needle sharing by drug abusers
-C virus infects liver cells, Creates damage, create specific response, Virus mutates, new response, new mutation
-Can lead to chronic liver disease
-Long-term lytic cycles
Treatment
-Reverse transcriptase inhibitor
Prevention
-No vaccine
46
Q

HIV

A

Made biological features
-Envelope RNA virus
-Glycoprotein spikes that mediate adsorption into the host cell
Clinical manifestations
-HIV-t4 cells decrease every year till below 200/ml which is AIDS
-AIDS
Mechanisms of disease
-spikes that attach to host cell
-Reverse transcriptase, integrase, protease
-Rapid mutation
-Formation of synctia
-can be lytic or latent
Transmission
-Sexual intercourse
-Transfer of blood or blood products
-Babies can be infected before/during birth/Breast-feeding
Prevention
-Safe sexual practices abstinence, Monogamy, barrier protection
-No vaccine
Treatment
-HAART- highly Active antiretroviral therapy
-Contains combination of reverse transcriptase inhibitors, protease inhibitors, fusion inhibitors and integrase inhibitors
-Can only slow progression to AIDS

47
Q

rhinovirus

A
  • associate with the common cold
  • sensitivity acidic environment such as the stomach
  • optimal temperature is in human nose
  • important for study for immunities, Because antigens have a wide variation of knobs and pockets
  • self-limiting
48
Q

Hepatitis A virus

A
  • cubicle picornavirus resistant to heat and acid
  • RNA virus
  • principal reservoirs are asymptomatic
  • fecal oral transmission
  • Most infections of clinical, flulike symptoms common -Jaundice occasionally
  • No specific treatment
  • Vaccine available
49
Q

Calcivirus

A
  • Norwalk agent(diarrhea in adults), Believed to cause one third of all viral gastroenteritis cases
  • transmitted by fecal oral route
  • acute onset, nausea, vomiting, cramps, diarrhea, chills
  • rapid recovery
50
Q

reovirus

rotavirus

A
  • cold like upper respiratory infection, enteritis
  • have unusual double stranded RNA genome
  • significant of diarrhea in newborns, calves, and piglets
  • wheel-shaped capsid
  • transmission fecal contaminated food/water
  • high mortality from diarrhea
51
Q

Prions and Spongiform Encephalopathies

A

Main biological features
-Prions-proteinaceous infectious particles, highly resistant to chemicals, radiation, and heat
-Mad cow disease in cattle, scrapie in goats
Clinical manifestations
-transmissible Spongiform encephalopathies- neurodegenerative disease with long incubation periods
-Creutzfeldt-Jakob Disease(CJD)- alteration of the structure of normal protein in the brain
Mechanisms of disease
-Prions
Transmission
-genetically endemic, contact with infected brain tissue or cerebrospinal fluid
Prevention
-the Avoidance of contaminated tissue
Treatment
-no known treatment, patients will die, ease symptoms