Microbio Exam 2 Flashcards
Hep C
Transfusion associated hep
Hep D
delta agent, only in pts with ACTIVE HBV
TB caused by
Mycobacterium tuberculosis
Big worry about TB is the spread of it
Often sneaky bc 90% of health infected pts
never become ill
Reservoir for Mycobacterium Tuberculosis
only HUMANS
transmission: person to person through Aerosol droplet
Prosectors warts
Cutaneous skin sx of Tuberculosis
Mycobacterium TB
Obligate aerobes
Rod shaped bacillis
M. TB
intracellular growth- alveolar macrophages
Harsh tx employed for Mycobacterium TB because:
Acid Fast Bacilli (AFB)
Myco TB
Ziehl-Neelsen or Kinyoun stains
Myco TB structures that create problem
remember, Acid fast
Mycolic acid-prevent dehydration, resist water
Cord factor
Lipoarabinomannan (LAM)- ROI-
Myco TB manifestation
Granulomas surrounded by macrophages, giant multi-nuc, fibroblasts, and collagen fibers h
Show on CXR 2-6 wks after infection
Latent TB
No risk to spread disease
Still treated
Reactivation or Secondary TB
Sign & Sx present
INFECTIOUS to others
may be present wks-months b4 diagnosis
Cough, wt loss, fatigue, fever, night sweats, CP
Lesions- caseous with . necrosis, erode and discharge TB bacilli into bronchi
Erode blood vessel and now spread via blood
Dx of TB
CXR
Skin test reactivity
Sputum stain/broth culture to detect Acid Fast bacteria
Rapid blood test- IFN-gamma
Myco TB screening
use purified Myco TB protein derivative in TB skin test
TB skin test
“Mantoux test”
Tx for TB
Extended duration 6-9 months
Chemo
Multi drug regimen
Prophylaxis for TB
Isoniazid for 9 months
do BCG (a tuberculosis vaccine)
in high endemicity regions
MAC
Mycobacterium avium complex
Acid- Fast
water loving- ubiquitous
slow growing
MAC
weakly gram (+) aerobic bacilli
MAC epidemiology
Ingestion of contaminated water or food
MAC
NO person to person transmission like TB
No isolation required
MAC
opportunistic Human pathogen
Now the leading cause of Non TB mycobacterium infections in HIV pts
MAC dz spectrum
Immunocomp
(middle aged/older males hx smoking)
-cavitary lesions resemble TB
MAC dz spectrum
Elderly female Non-smoker
-patchy or nodular CXR
Lady Windermere’s syndrome
MAC and AIDs
blood spread- no organ spared
immune system collapses
HAART and abx proph makes infection less prevalent in HIV (+)
MAC dx
Microscopy to reveal Acid-Fast and culture
Sterile site isolation of MAC
CXR
PCR- 16S rRNA sequence
Measles
multiply in Respiratory and Lymph nodes
Measles
Prodromal
High fever
3 C’s (cough, conjunctivitis, coryza)
Measles
KOPLIK spots and 3 C’s
Measles
Rash phase-sickest
Rash 3-4 d after prodrome starts
Below ears-spreads down
lesions become merged
Highest fever
Measles complications
PNA (most deaths)
Bacterial superinfetion
Diarrhea
CNS involvement- Acute sx-atic Encephalitis!!
Measles CNS complication
SSPE- Subacute sclerosing panencephalitis
Measles hosts
M for MONKEY
Humans and Monkeys
Measles
no healthy carrier state
Measles transmission
Respiratory droplets-highly contagious
Measles dx
Rash and/or Koplik spots
Serology
FA (fluorescent antibody test) from HEENT- Multniucleated giant cells
Measles prevention
MMR vaccine
-b4 school
15 mo:1st dose
4-6 yo: 2nd dose
*high risk if exposure deemed likely, can vaccinate under 15 mo
MMR vaccine
3rd booster now recommended for some
MMR vaccine
Live attenuated
Rubella (german measles)
“little red”
Mild exanthematous dz
Rubella
requires close and PROLONGED contact
Rubella
children often escape infection- the real scare is with CONGENITAL RUBELLA SYNDROME
CRS Congenital Rubella Syndrome
Maternal infectoin during 1st trimester of pregnancy Cardiac- Pulm stenosis, PTA Eye- cataract, galucoma Hearing loss CNS
CRS Congenital Rubella Syndrome
the earlier mother affected- the more severe for child
i.e. first month: 50% chance of CRS
Rubella tx and prevention
MMR vaccine
DO NOT GIVE VACCINE TO PREGNANT
May proved IVIG (immunoglobulin) as prophylaxis if pregnant mother exposed in first trimester
Rubella tx
Symptomatic
HSV
humans are only reservoir
HSV spreads
in abscence of immune response
HSV dx
Ballooning patholody Tzanck smear! FA- Fluor Antibody for viral antigens Culture in HeLa, Hep-2 cell lines PCR to detect HSV Antibody tests to reveal HSV1 and 2
HSV tx
Acyclovir or Valacyclovir
HSV tx
Acyclo and Valacyclo
Thymidine kinase phosphorylates AVC- viral DNA replication bc lacks 3 OH group and cannot polymerize more bases
Chickenpox
Asymmetrical
vesicular
Chickenpox
Replicates in regional lymph nodes
Replicates in liver and spleen
Chickenpox
Primary viremia 4-6 days after infection Secondary viremia (rash) 10-14 days after infection
Chickenpox
humans only reservoir
Chicken pox transmission
Respiratory secretion
Conjunctiva
Vesicles
Highly contagious
Chicken pox incubation
15 days
pt most contagous 1-2 days before lesions, and 4-5 days after
Chicken pox tx
DO NOT GIVE ASPIRIN (reyes syndrome risk)
Acyclovir is effective
High risk: Immune serum VariZig (immunoglobulin)
Chickenpox vaccine
Varivax (live)
VariZig for high risk
Shingles
Redness –> papules in 24 hour period
fever, anorexia
Shingles prevention
Zostavax (over 50YO)
Shingrix
HHV 6
Roseola Infantum
6th dz
HHV 6 Roseola Infantum
Fever followed by rose colored rash
HHV 6
fever 2-5 days
High fever w/o any obvious source
HHV 6 dx
Antibody by EIA
PCR
HHV 6 tx and prevention
nothing
Parvovirus
5th dz
Erythema infectiousum
infectious with 5 hands, 5th disease, slapped cheek with a HANG 5
Parvovirus
pet dog with HAND
5
5th dz
Parvovirus
Mild sx-fever, ha , malaise
Followed by SKIN RASH (Slapped cheek)
Resolves in 1-2 wks
Parvovirus
rash may involve limbs and trunk
ADULTS: Arthralgias!!! may only have this without any other sx
Parvovirus dx
Anti B19 IgM antibody
Parvovirus Tx and prevention
Most make full recovery on own
NSAIDs for relief
Immunoglobulin for Anemic pts
HPV prevention
Vaccines !!!
Gardasil
M and F ages 9-45
Scabies
small mite with short legs
Female scabies
fertilized on skin surface
burrows
life cycle in 5 wks- dies in burrow
Male scabies
shorter lifespan remains on skin surface OR shallow burrow eggs laid under skin larva emerges from egg after 4 days adult mite develops 2 wks after hatching
Pediatric Scabies
similar to Norwegian, but lesions may be blood filled
Dx scabies
Apply mineral oil, scrap lesion, visualize microscopically (whole mite, mite parts, eggs/fecal pellets)
Tx of Scabies
5% Permethrin cream (single app) wash off after 8-14 hrs
Ivermectin (does not kill eggs)
Pubic lice
Nits (eggs) cemented to hair
ID by visualizing louse or nit
Tx of Pubic lice
Permethrin
Pediculosis
“Lice”
can be Capitis: head or
Humanus:body
Pediculosis “lice” pathogenicity
Bite irritation (blood sucking parasite)
“Vagabonds dz”
years of Lice infestation- darkened thickened skin
Tx of Pediculosis Humanus (body lice)
Permethrin
Pulex irritans (human flea)
laterally compressed
short spikes on legs allow attachment to host
Pulex irritans (human flea)
Parasite-need blood to survive
Inject saliva during blood meal, possesses 15 stubstances which initiate ALLERGIC RESPONSE
Pulex irrritans (human flea)
Allergic response
Rash
Tx: 1% Hydrocortisone cream, stop scratching, Antihistamine
RMSF
Tick borne Brown dog tick Rickettsia Ricketsii Gram (-) Obligate intracellulra
RMSF
can be FATAL if not treated in first few days of sx
RMSF sx
2-14 days after tick bite
(usually painless bite)
SUDDEN ONSET fever and HA
RMSF early nonspecific sx
Fever, HA, n/v, abdominal/ muscle pain, lack of appetite, conjunctival infection
RMSF 2 types of rash
type 1
Small, flat pink itchy spots on WRIST, FOREARM, ANKLES (spread to trunk and palms, soles)
2-5 days after infection
RMSF 2 types of rash
type 2
Red-purple spotted petechial, pinpoint hemorrhage
6 days after
YIKES- sign of SEVERE and LATE dz
RMSF
Small, flat pink spots WRIST/ANKLE (2-5 days)
treat before rash gets to
Pinpoint hemorrhage (6 days)
Dx of RMSF
Detectable antibody titers are not visible for 7-10 days post infection
difficult to detect until dz is in late stage
Gold standard dx RMSF
Indirect immunofluorescense with a R. Rickettsii antigen
2 samples, 2-4 wks apart
Tx for RMSF
DOXY within 5 days of sx
Pregnant: Chloramphenicol (beware aplastic anemia)
Trypanosomatids
T. Brucei: African sleeping sickness
T. Cruzi: Chagas
T. Cruzi
Chagas
Vector: Triatomine bugs “kissing bugs”
T. Cruzi
transmitted through- feces of kissing bug, blood transfusion, organ transplant, congenital
T. Cruzi lifestyle
Trypomastigotes –> Amastigotes
Amastigoetes then replicate via binary fission and go back to Trypomastigoses-release into circulation
Trypomastigoes
ingested during bloodmeal
Chagas- 2 stages
Acute vs. Chronic
Acute Chagas
Nonsp sx (fever, fatigue, rash, n/v/d) + 2 BIG SIGNS Chagoma (circle next to eye) Romana's sign (swelling of eyelid near parasite entry)
Chronic Chagas
Can be asx for years- even life, THEN Muscle and Nerve degeneration--> necrosis Chronic inflammation Cardiac effects Intestinal enLARGEment
Heart comp more common than intestinal comp
Chagas dx
Parasite under microscope
- Trypomastigotes in Acute phase
- Amastigotes in Chronic phase
Tx of Chagas dz
Benznidazole
Links to Epstein Barr Virus
Mono
Burkitt’s Lymphoma
Infectious Mononucleosis (IM)
Incubate 1-2 months
Oropharynx–> Lymph nodes
Mono
B cell infection - spread through lymphatic system
Mono prodrome
3-5 days of HA, fever, malaise
Mono presentation
Sore throat, symmetrical lymphadenopathy, FEVER, Hepatomegaly, increased liver enzymes, Jaundice
Mono sore throat
Hard and soft palate lesions
Increase in both T and B cells
Atypical lymphocytes “Downey cells” in circulation
Mono and T cell response
T cell response controls and halts infection (also cause of most of pt’s sx)
Mono
virus found in saliva for about one month
EBV
Mono dx
Heterophile Antibodies!!!
Mono tx
Symptomatic
Mono
Penicillin reaction rash often occurs in pts
CMV-Cytomegalovirus
similar to EBV (mono), but does not produce Heterophile antibodies
CMV
Most problematic for: Transplant pts, Immunocomp Pregnant
CMV
children with minor colds may be source
CMV tx
Ganciclovir and Immunoglobulin (Cytogam)
Mumps
Symptomatic
MMR vaccine
Lyme dz
Borrelia Burgforferi
Dz progression similar to syphilis
Lyme dz progression (3 stages)
- Acute localized Erythema migrans- “bullseye” and flu like sx (fades in less than a month)
- Subacute disseminated dz- ARTHRALGIAS and flu like sx
Secondary annular skin lesions
Hepatitis
Meningitis
Facial palsy
Conjunctivitis - Chronic- MSK manifestations, worse Arthritis
Lyme dz Reservoir
Small mammals- rodents, rats, mice, birds (tick transmission essential to maintain cycle)
Lyme dz Dx
Serology- EIA + Western blot
False + tests with Lyme dz
Syphilis, mono, Lupus, RA, oral infection w spirochetes
Tx of Lyme dz
Amoxicillin or
Doxy 10-21 days
Vaccine for Lyme dz
LYMErix (was available?)
New vaccine targeting 6 most common Borrelia species
for Lyme dz
Pre-exposure proph with Monoclonal antibodies (passive immunity)
Hep A and E
only Acute
Hep B, C, D
can be Acute or Chronic
Which types of Hep offer pre/post exposure immunization?
A, B, D
Hep A
Excreted in feces
Food and water borne
Poor hygiene
Hep A
Dz typically mild
Entry thru intestine after ingestion
Many ASYMPTOMATIC infections occur
HAV dx
IgM antibody by ELISA
Hep A tx
Bed rest
Reduce actiivty
PO fluids
Avoid: drugs, alc, anesthesia
Prevent Hep A
Handwash
Avoid contaminated food
Post exposure prophylaxis with immunoglobulin
VACCINE available
Hep B
Chronic –> Liver CA
Hep B Antigens
Pay attention to third letter
HBs: surface
HBc: core
HBe: surface that tells us pt is INFECTIOUS
Hep B
Double walled “Dane particle” is the infectious form
Hep B spread
needle sharing, acupuncture, ear piercing, tattooing
Chronic Hep B
major source of spread
when pt is Asymptomatic
Mother has HBeAG (e is third letter) greatest risk of spreading
Populations at risk for Hep B
Healthcare workers
IVDU
Hep B sx
Incubate 50-180 days
Insidious onset: fever, rash, symmetrical arthralgias
Subclinical infection of Hep B (nearly or completely asymptomatic)
Anti- HBsAg
self limited in most adults
Hep B
we always vaccinate BABIES
B for BABIES
bc 90% of perinatal and pediatric infections –> CHRONICITY
Complications of Hep B
Hepatocellular Carcinoma
Sign of Hep B- HALLMARK of initial ongoing infection
IgM anti-HBc and HBsAg
Past infection of Hep B
IgG anti- HBc
Chronic infection of Hep B
IgG anti-HBc and HBsAg
Probable chronic infection of Hep B
HBeAg and HBsAg continued detection
Hep B Tx
Chronic: PEG-interferon
Subunit vaccine available
Immunoglobulins for prophylaxis
Newborn infants of HBsAg + moms: get immunoglob prophylaxis + Hep B vaccine at birth
Hep D virus
needs Hep B in order to replicate
Hep D
increases the severity of Hep B
“Fulminant Hep” more likely with Hep D
Hep D dz
ELISA for DELTA antigen or antibodies
Hep D prevention
the vaccine for Hep B prevents both B and D
Supportive therapy
PEG interferon to suppress active viral replication
Hep C
If not type A or B, 90% of Hepatitis cases are this
Hep C
Hallmark for CHRONIC
post transfusion
Hep C
Chronic –> Liver cirrhosis and failure
Hep C
transmission not well understood
Dz onset hard to pinpoint
Risk factors for Hep C
Anything with needles
Organ transplant
Contact w health care providers
Factors that promote Hep C progression to Chronic
Alcohol use Infection at age <40YO Male sex Co-inf w Hep B HIV
Hep C dx
Enzyme immunoassay against Hep C
Seroconversoin 24 wks after infection
OFTEN ESCAPE DETECTION
What is recommended to detect Hep C since it often escapes diagnosis?
Direct assays
Hep C tx
Direct acting antiviral (DAAs)
Combo regimens
Virus protease or poylmerase inhibitors
Hep C tx
a-interferon
PEG-interferon for some genotypes
Some regimens do not require interferon
Hep C may lead to needing a
transplant
Two main causes for Liver transplant
Cirhossis
Liver CA
HIV sx
Asx or Sore throat, swollen lymph nodes, mimicking Mono
HIV transmission
early stages when pts are unaware is when high levels or virus are circulating- HIGH transmission risk
AIDs
(stage 3 HIV)
CD4 <200
Opportunistic infections take over- CA, Kaposi’s sarcoma, PJP, MAC infection, CMV dz, candidiasis thrush
Description of HIV agent
Makes copy of itself and inserts into Human chromosome
Host treats it as any normal gene, cant be recognized
Human retrovirus- RNA genome- two copies of RNA virion
HIV agent
RNA genome- 2 copies
Enveloped
Reverse transcriptase- RNA dependent DNA polymerase
RNA–> DNA, then entered into human genome
Target for HIV tx
Reverse transcriptase
HIV replication
Infection of cells w CD4 and Chemokine co-receptor at surface
Th monocyte, macrophage
Reverse transcriptase of viral genome-integration into hose
Cytpopathic effects of HIV
T (helper) cell loss
and profound immunosupp
Direct virus killing and/or Apoptosis of immune cells
“swarms” group of mutant viruses that develop
“swarms”
groups of mutant HIV that develop
can multiply rapidly, complicating tx (always morphing to escape med)
Why we need COMBO therapy
HIV-1 and HIV-2
HIV-1: more common worldwide
HIV-2: West Africa
HIV-2 (W. Africa)
less easily transmitted
slower progression to AIDs
resistant to NNRTIs
HIV dx: detection of Antibody in patient
2 step process
- EIA screen
2. Western blot (confirmation)
HIV dx: direct test
Reveal presence of virus RNA or protein antigens
NAT- Nucleic acid test are used to detect and quantify virus
Check with donated blood for HIV
Antigen p24 or RNA genome by PCR
Rapid HIV test
new 20 min test
OraQuick Rapid HIV-1/2 antibody test
(estimated that 280K ppl in US are infected but do not know)
HIV tx
Combo Reverse transcriptase inhibitors Nucleoside analogs (AZT, ddI, ddC) Non-nucleoside analogs Protease inhibitors- stop maturation of viral assembly Fusion-penetration inhibitors
Viral load
most tests can detect as low as 50 copies/ml
Persons w HIV: may monitor every 90 days
Poliomyelitis
Asymmetric flaccid paralysis
destruction of motor neurons in spinal cord
Poliovirus
Picorna virus
Clinical sx of Polio
- Inapparent- Asx to minor malaise
- Abortive illness
- Nonparalytic poliomyelitis
- paralytic poliomyelitis
Post polio syndrome
paralyzed decades ago Now: muscle weakness, pain, fatigue 30 or more years after paralyzing polio Not contagious- not detectable levels Remaining neurons are collapsing d/t overuse
IPV- Inactivated polio vaccine
we now use E-IPV, enhanced
Injected
Virus is killed
Prevents dz (paralysis), not infection
Only polio vaccine used in US
IPV
Arbovirus
West Nile virus
Ticks and mosquitoes
(break chain of transmission by going after these guys)
West Nile clinical sx
Mostly NOTHING
if sx show, very serious case: still can’t treat though- only make pt comfortable
West Nile
prevention and educatoin extremely important b cno treatment
West Nile sx in severe case
AMS, confusion, fever, HA, vertigo, photophobia, n/v,personality change, seizures
Recovery may be complete or long term deficits
West Nile
1 cause of Viral encephalitis in US overall
West Nile dx
Antigenic cross rxn
MAC-ELISA is what we use: look for IgM
If pt had recent (9 mo) vaccination against Yellow fever and/or Japanese encephalitis,
IgM may be detectable for up to 9 months after vaccine, can be false (+) for West Nile
If suspect West Nile
start Acyclovir
in case it is Herpes Simplex virus
Arbovirus (west nile) prevention
do not keep sitting water around
Zika
teratogen
GBS
Guilliane Barre syndrome
Rabies
virus replicates locally but heads for nervous tissue
Rabies, Polio, HSV
travel back and forth from body– nervous tissue
Rabies
Incubate 2-16 wks
5-6 days fatal course when overt sx appear
Rabies prodrome
mild fever, pharyngitis, HA, burning, pain, increased sensory sensitivity
Excitatory phase of rabies (mad dog)
anxiety, hydrophobia
Paralytic phase
coma, hypotension, death
Cryptic Rabies
contact with Rabid animal
virus can get thru skin
Rabies
only instance where we immunize after the bite
3 immunizations
99% cure
Rabies vaccine
HDCV + Hyperimmune serum AFTER contact w reservoir
Malaria
mosquito born
Malaria most common causative agents
Vivax and Falciparum
Malaria
Human phase and mosquito phase
Malaria
First: Sporozoites are injected by mosquito’s saliva during blood meal
Sporozoites then travel to liver where asexual division occurs–> Schizogony cycle begins (rapid cell division)
-Merozoites are released from Schizogony phase
Vaccine target for malaria
Sporozoites (what is release by mosq saliva)
Merozoites (made from Schizogony in the liver)
can infect other liver cells or RBC
Once in RBC, Merozoite –> Trophozoite
As tropho age, they can develop into Amoeboid tropho and release into bloodstream, infect more cells
Schizonts are multinucleated cells that produce
Merozoites
Some merozoites can even develop into Gametocytes that do not rupture, BUT
mosq can then ingest the gametocytes and more reproduction happens inside the mosq
Malaria
Organism uses up Hgb
Fever and chills d/t Pyrogenic waste after rupture of RBC
Malaria
Pyrogen travels to hypoth and causes increase in thermal set point
Tumor necrosis factor- TNF; inflammation- intensifies symptoms
Malaria
1-2 hours of severe shivering and high fever
Malaria sx mimic others
Fever, vomiting, myalgia, Anemia (d/t RBC destruction), hypotension
Untreated: coma, renal failure, resp distress, death
Resistance to Malaria
Sickle cell (virus doesnt want the messed up Hgb) Duffy antigen (W. african black persons lack antigen, resistant to VIVAX form)
Duffy antigen
resistant to VIVAX
Malaria vaccine
RTS, S (Mosquirix) somewhat eff against Falciparum 4 injections low efficacy Req boosters
VIVAX
Benign tertian malaria
Rarely fatal
Incubate 9-15 days
infects YOUNG RBCs
VIVAX
fever every 48 hours lasting 2-6 hours (d/t rupture of schizonts)
chills and shaking every 10-15 min
Relapse common d/t activation of Liver Hypnozoites, can be 3-5 years after initial dz
Sickle cell protection against what form of Malaria?
Vivax!
Vivax dx
Giemsa stain
Enlarged RBC w/Schuffner’s dots
Stipling
Vivax tx
Chloroquine
Quinine
Doxy
Primaquine
Falciparum
RBC of ANY age affected
VIRULENT- multiplies rapidly
Fever very high d/t high # of parasites
BLACKWATER FEVER
“Blackwater fever” in Falciparum
high levels of free hgb
auto-immune rxn host destroys kidney tissue
Chills, fever, rigor, DARK TO BLACK URINE
Falciparum crappy scary effects
Capillary obstruction bc infected RBC stick to capillary linings
Cerebral: hemorrhage, mania, convulsions, death
GI: freq vomiting
Algid*: skin is cold but internal temperature is high
Falciparum is very crappy BUT
no relapse d/t no Hypnozoite
Vivax and Ovale
relapse occur
Duffy antigen
Vivax
low incidence in W Africa d/t Duffy negative people- dont have this antigen
Main cause of Malaria resistance
efflux pumps
Tx for Malaria
Chloroquine or Artemisinin
Atovoquone/proguanil (more expensive)
Babesiosis
Nantucket fever
Babesioss/Nantucket
deer tick
Similar sx to Malaria
Small pinpoint lesions
Babesiosis/Nantucket is more problematic in
Immunocomp
Asplenic
Babesiosis/Nantucket is often a co-infection with
Lyme dz
Babesiosis similar to what form of Malaria?
Falciparum (but less severe)
Babesiosis is known for what morphology of RBC?
Cross like
Tx ofBabesiosis
Clinda and Quinine
E Coli
Bacillus
Listeria
Gram + Coccobacillus Hot dogs in summer GI Facultative INTRAcellular all up in your cell Lysterlysin O
Group B strep
Strep agelecta
Cocci
H. influenza
Listeria
Coccobacillus
Hep tx
Hep A: IgM
Hep B: Hbsurface antigen
Hep C: look for RNA (treat with DAA)
Hep D: Delta antigen
HIV
EIA and Western blot
HIV blood test
direct testing for RNA
Vivax
Stipling
Schuffner
Falciparum
Maurer’s cells
Maury is falci