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283 Cards in this Set
- Front
- Back
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Hallmarks of Mono
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EBV Incubates 1-2 months
Polycolonal Espansion of B cells kept in check by t cells Usually kids in their 20s who present with sore throat, lymphadenopathy, and hepatosplenomegaly |
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What cells are seen with EVV/Mono?
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B cells multiply first
:atypical: lymphs are t cells that cause sx |
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Morphology of EBV
Family, Enveloped?, genome? Spread? Chronicity? |
Herpesvirus (gamma)
Enveloped dsDNA Spread in saliva, virus found for 1 month Some people harbor latent virus in pharynx that keeps lymphs infected |
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What disease has "downey cells"
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EBV (Infectous mono_)
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What antibodies screed for in regards to infectious mono?
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Heterophile antibodies (transient)
EBV antibodies are permanent |
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What drug should be used in caution with mono patients? What other sequela?
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anpicillin known to cause rash in many
can get spleic rupture, chronic fatigue and malignancies like BURKITTS Lymphoma (c-myc) |
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Most common infection of a fetus? Who else is affected by it?
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CMV
major case of MM in HIV and transplant patients |
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What betaherpesvirus replicatres only in fibroblasts cultures of humans, but in vivo epithelial cells? What is characteristic appearance?
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CMV - "Owl's Eye" inclusions
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How is CMV transmitted?
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Blood, blood saliva?, semen, urine, and donor organs.
No seasonalily, but higher in poorer areas |
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How might you determine CMV from EBV?
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CMV will be much older patient and likley immunocompromised
They will have abnormal atyptical lymphs, but heterphile negative antibody BOTH can establish latent infections and can present similarily |
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What is CMV risk to fetus of infected or reinfected mom?
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Greater risk with primary onfection most kids (90% are asymptomaic or mild) 10-20% of those with mild infections will suffer permanent brain damage
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What transfustions/transplants have the greatest risk for CMV reactivation?
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Kidney, heart and liver carry a 70-90% risk, Blood has a 2% risk with a single infusion
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How is CMV Diagnoses in a newborn?>
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It is part of the TORCH series and most common of the group
You can see giant cells in any organ or expelled int he urine, or you can look for IgM Elisa |
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What is the morphology of Mumps?
Family? genome? Enveloped? Features? |
Paramyxovirus
-ssRNA Enveloped Spikes with NH and capsid |
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How will mumps present?
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Febrile kiddo with bilateral parotitis
Can cause Ortchitis But 30-40% can be asymptomatic |
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What are the limitations to the mumps vaccine?
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Cant give to those with egg, neomycin or immuncomp/preggers.
Mumps efficacy is the lowest of the MMR vaccine with perhaps 10% of total recipients remaining unprotected after two administrations |
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Why are we seeing mumps still?
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2006 – over 3, 000 cases were reported, centered in the Midwest, with
most cases in vaccinated patients Investigation revealed the vaccine is effective against the G strain responsible for the outbreak This outbreak may have revealed systematic failure in our MMR vaccination method and the need for a routine third boosting Outbreaks continue to be reported, typically linked to foreign travel and non-receipt of vaccine |
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What are the two genera of Retroviruses? How do they differ and what are the subtypes?
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lentivirus (HIV) - Helical capsid
-Two types HIV-1 and HIV-2 (less virulent) Oncovirus (HTLV)- infection with strains 1 or 2 (of three possible strains) results in immortalization or transformation of target cells |
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What are the three top genes in the nine gene HIV-1 genome?
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gag
pol Env |
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What does the gag gene code for?
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encodes a precursor that is cleaved into four functional
nucleocapsid proteins: p7, p9, p17, and p24. |
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What does the pol gene code for?
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encodes a precursor that is cleaved into viral enzymes: protease
(p10), reverse transcriptase (p51, p64), and integrase (p32). |
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What does the env gene code for?
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encodes a precursor that is cleaved into two envelope glycoproteins
gp41 and gp120, allowing viral attachment and fusion to CD4 cells. |
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How does HIV Attach to host cell? How about FUSE?
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HIV-1 gp120 attaches to CD4 located primarily on monocytes,
macrophages, T cells, and bone marrow progenitor cells. Association of the CD4-gp120 with a co- receptor is also required. The co-receptor is a chemokine receptor – CXCR4 or CCR5. needs gp 41 to fuse |
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When are gag and pol proteins released in the HIV life cycle? what is the consequence?
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After the virus attaches ans fuses, the HIV genome is uncoated and releases gag and pol. This then allows the RNA to be converted to DNA and be integrated into the genome. becuase this is a quick and dirty process a lot of errors are made causing multiple mutations.
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How does integrase deside where to place DNA from HIV?
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It is random
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Criteria to say a patient has AIDS?
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HIV + Plus:
-othr adis definfing oportunistic infection to cancer or CD4 <200 or Lymphs <14% |
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How is the HIV virus spread?
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Even though body makes antibodies to gp120 to coat the virus, the virus is still functioning and infects the macrophge that eats it and also helps it disseminate throughout the body :(
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What protein markers define a positve western blot for HIV?
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A band at p24,p31, gp41,gp120, gp160
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How do Nucleoside RT inhibitors work? Non-nucleoside analogues
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Both are Any of a group of antiviral drugs that inhibit the viral enzyme reverse transcriptase and are used in the treatment of HIV infection.
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How do protease inhibitors work?
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They block processing of viral materials that were made int he nucleus so that they aren't viable
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How do entry /fusion inhibitors work? How about Integrase inhibitors?
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Self explanatory: recognize as part of HAART
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What are the 7 classes of antiretrovirals?
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Nucleopside RT inhibitors
Non-nucleoside RT inhibitors Protease Inhibitors Fusion/entry inhibitors Integrase inhibitors Maturation Inhibitors Antisens "drugs" (retroviral vector that contains HIV antisense genes) |
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How does the action of HTLV compare to HIV?
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they are NOT cytolytic and can persist inside host cells for years
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What are the consequences of HTLV-1 Infections?
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Patients are asymptomatic generally but can progress decades later to ACUTE T-CELL LYMPHOCYTIC LUKEMA which is a malignant proliferation of CD4+ T cells
Some cases have bilateral tropical spastic paraparesis = bilateral progressive weakness of lower limbs with some stiffness, some sensory loss, and possible hyperactive reflexes |
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What gene foes HTLV have that HIV doesn't and what does it do?
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TAX gene that transactivated genes for IL-2 and IL-2 R (Stimulates T cell proliferation and diff of B and NK cells)
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What is the role of IL-2 and IL-2R and its impact on HTLV-1?
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IL-2 and IL-2R are needed for T cell proliferation, and is normally
produced by the T cell upon antigen stimulation. HOWEVER in HTLV-1, Production of IL-2 and IL-2R without antigen stimulation results in uncontrolled clonal proliferation. |
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How is HTLV-1 usually detected?
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Detection of HTLV-specific antigens or antibodies via ELISA.
Peripheral blood smear shows atypical lymphocytes. Elevated WBC count as high as 100,000 cells/µL. Patient history is helpful. |
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Where is HTLV-1 virus endemic? How is it primarily transferred?
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japan
Caribbean Central Africa and Blacks in the SE United states (Low) IV drug use and blood transfusion, sex. Incidence on the rise |
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What are the therapies for treatment of HTLV?
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Lymphoma Chemotherapy
Combo INF-a and AZT (although usually fatal regardless of treatment). |
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What treatments for HCV?
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NO EtOH or Hepatotoxic Drugs
Give Intrafuron Ribaviron and NS3/4A protease inhibitor May require liver transplant |
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What is cool about HGV?
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Coinfection with HIV ssems to dcrease CCR5 expression on leukocytes, increase chemokines and reduce mortality
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What treatments for HAV?
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Immune Globulin
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What treatments for HBV?
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Adefovir dipivoxil
entecavir interferons lamivudine |
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What are the the clinical signs of Viral Hemorrhagic Fevers?
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fever, hemorrhagic manifestations, thrombocytopenia, shock, and
neurological disturbances. |
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What are the the clinical symptoms of Viral Hemorrhagic Fevers?
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fever, fatigue, dizziness, muscle aches, loss of strength, and exhaustion, rash
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Which host cells are infected with Viral Hemorrhagic Fever?
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Macrophages and Dendritic Cells
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What are the flavaviruses (5)? How do they get inside cells?
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Antibodies facilitate the viral uptake
Flavaviruses: West Nile St. Louis Enceph Hep C +Dengue Virus +Yellow Fever Virus |
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What are the Hosts and vectors for Dengue
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host is primate & Humans
Trnasmission is Aeded aegypti mosquitp |
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Describe presentation of primary Dengue Fever
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Acutely nonspecific fever, aches, pains and lympadenopathy and leukopenia. Rashe develops, fades, and second rash on limbs and face appear with desquamation (resolves in 2 weeks)
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Describe presentation of a secondary Dengue Fever infection
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high fever, weakining and rupture of vascualture (petechiae, purpura and ecchymosis), loss of plasma leads to increase hct and shock, thrombocytopenia
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Infection with Dengue 1 is managed by the body how?
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Body forms neutralizing antibody and CLEARS the virus
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Infection with Dengue 2is managed by the body how?
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Non-nutralizing antibodies promote uptake of the virus by macrophages anc activates T memory cells and causes inflammatory/cytokine response
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True or false: There is cross immunity among the four dengue viruses
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False
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What are Dakar and 17 D?
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Two strains of Yellow fever virus
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Who gets yellow fever and how is it transmitted?
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All ages but moreso in south american and central africa Males more than Females
Monkey ahd humans are the hosts Aedes and Haemagogus are the mosquito vectors |
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Describe infection with yellow fever
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biphasic
Acute: Generaly sick, fever, ha, n/v, RED Tongue, flushed face and red eyes (days 3-4) Toxic Phase (In 15% of Patients) Return of fever, JAUNDICE, GI hemorrhage with black vomit, can disseminate to other organs causing widespreas hemorrhage - 50% die in a week! |
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What cells are attacked with Yellow fever?
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Kupffer cells and hepatocytes with higer propensitiy. You see CONCILMAN bodies on biopsy
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Is there vaccine for yellow fever?
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Yes. LIVE attenuated YF-Vax for the 17D strain
Given to kids and imunecompetent adults >9 months. Once dose effecteve for 10+years |
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What is unique about the bunyavirus structure?
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Enveloped -sense RNA
has G1 and G2 glycoproteins Segmented genome L: RNA-dep RNApol M: G1, G2 S: Nucleocapsid Replication in cytoplasm and virions release via exocytosis or cell lysis |
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What is the genius and family of Rift Valley Virus?
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Bunya and Phlebovirus
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What are the host. reservoirs and vector for Rift Valley Virus Fever? Where is it endemic?
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Host = Livestock
Resivoirs = humans Vectors = Mosquitos (Aedes, Culex, Erethmapodites) East and southeast africa primarily |
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How does Rift valey Fever present?
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Asymptomatic or mild fever with Flu like illness + possible hepatitis. Rarely can progress to hemorrhagic fever, shock encephalitis and ocular disease (20% with 2nd Viremia). Spreads/worse with second viremia
The major problem is for livestock that die and abort pregnancies |
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Is there a vaccine for Rift Valley Fever?
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Yes for livestock and one in clinical trials now for humans
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How is Hantaan virus transmitted?
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Robovirus = ROdent-BOrne
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What does Hantaan virus cause?
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Hemorrhagic fever with renal syndrome
Inflammation of the retina (kidney failure and brusing/bleeding) |
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How is Hantaan similar to RVF?
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Primary Viremia infecets cells
Secondary Virenmia causes symptoms |
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Where is Crimean-Congo Hemorrhagic Fevers Seen?
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SE Europe, asia and africa M>F, mortality 30% Bioterorrsism threat
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How is Crimean-Congo Hemorrhagic Fever spread?
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Major vecot is the Hyalomma marginatum TIC
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What is the morphology of the Arenaviruses?
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Enveloped ss RNA with 2 ring segnmented genome
L: - sense pol S: ambisense, N protein +G1 and G2 BUDs from membrane |
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Where is Lassa virus found and how is it primarily transmitted?
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West Africa
Rodent borne = Mastomys natalensis Can get from ingesting fod contaminated with urine or PERSON to Person |
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Describe the clinical persentation of lassa virus?
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Insidious:
Fever, ha, dry cough, back pain, v/d somtines macopapular rash and photophobia |
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What is a potential long term complication of Lassa virus
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1/3 of patients have some hearing loss
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What are two Filovirdae virus and what is the morphology of this genus?
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Ebola and Marburg
Filamentous, pleopmorphic -ssRNA enveloped |
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Where is Marbug virus seen and what is the resivoir? Ebola
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Endemic to Africa
Fruit bats likely the nature resivoir Ebola is exactly the same |
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What is unique about the Filoviruses?
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They often cause SEVERE fatal hemorrhagic fever, shock, hemorrhages and sever thrombocytopenia. The virus rreplicates causing severe tissue necrosis and viremia pesists, macrophages release mediators that smimic septic shock reulting in DIC and death
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What is the only Viral Hemorrhagic Fever virus that has avaccine?
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Yellow Fever
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Lassa, Hantaan and RVF virus can have morbidity and mortality reduced how?
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Ribavirin and supportive care
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What is the scientific name for malaria?
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Plasmodium
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What is the scientific name for Babesiosis
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Babesia
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When are you more likely to get malaria?
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Traveling abroad (SA and Africa) and at NIGHT anophalies misquito bites
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What is the life cycle of malaria in the human?
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Sporozoites in mosquito saliva are injected during a blood meal.
Sporozoite migrates to the liver and exoerythrocytic (EE) schizogony (asexual division) begins. EE merozoites are produced by and EE schizont; escape from the hepatic cell to infect erythrocytes. Erythrocytic stages include the young trophozoites (ring or signet forms) and older trophozoites (amoeboid forms and schizonts). Erythrocytic schizonts (segmenters) are multinucleated cells and produce erythrocytic merozoites. Infected RBC ruptures, merozoites escape to invade new cells. Schizogony begins again, or gametogony is initiated (microgametocyte = %, macrogametocyte = &). Another mosquito ingests the gametocytes during a blood meal and fertilization results in a gamete, ookinete, and then an oocyst. Sporogony occurs within the oocyst (ie, produces sporozoites) and sporozoites migrate to salivary glands of the mosquito. |
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what are the RBC stages of malaria (4) life cycle?
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Throphozoite
Schizont merozoite gametocyte |
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what are the exoerythrocytic (liver) stages of malaria in the human
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Sprozoite invades hepatocyte
trophozoite schizont merozoiteescapes from the liver |
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What is the infective stage of malaria?
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Female anopheles injects SPOTOZOITES
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What phase of malaria invades the RBC and ruptures?
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Merozoites
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What is the ring stage in the RBC with maaria?
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it is a young trophozoite
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What is the schizont?
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AKA segmenter, the second phase of RBC malaria...
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What do merozoites change into?
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Mico- and macrogametocytes which are are ingested by the mosquito when biting
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How many micorgametes from a microgametocyte?
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8
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How many macrogametes from a macrogametocyte?
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1
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Where to micro and macrogametes meet up to fertilize? What happens mect?
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In the the mosquitos gut
The oocyts that forms resulys in sporozoites which migrate to the salivary gland of the mosquite which is how they infect |
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What two factors impart resistance to malaria?
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Sickle cell anemia:Abnormal hemoglobn makes it difficult for heterozoites to use
and LACK of a duffy antigen (vivax) means that there is a missing IL-8 receptor which decreases the infectivity |
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What population is most likely to NOT have a Duffy antigen?
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West Africans
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Which malaria is considred benign because it won't kill you?
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Plasmodium vivax
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What is the incubation for P vivax and what does it infect?
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Incubation 15 days
Infects young erythrocytes |
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What are fever and chill associated with in p. vivax?
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Rupture of the schiznot infected erythrocytes that release mediators/pyrogens that also change the hypothalmus set point
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What malaria form can recur within 5 years? What stage is responsible
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P Vivax - hypnozoite stage
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What is the resivoir for p Vivax?
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Humans only
Can get from blood transfusion |
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How can you ID P Vivax?
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Do a giemsa stain, look for the diagnostic stages in the erythrocytes (schuffners dots) and know that they are larger then the RBCs around them
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What are the drugs for P. vivax?
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"quines"
Chloroquine quniodine primaquine |
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What malaria form is very deatly
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P. falciparum
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What is the incubation for P. falciparum? What cells does it infect?
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8-11 day incubation
invades RBCs of ALL ages so it causes more loss and damage |
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What is the resivoir for p Vivax?
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Humans only
Can get from blood transfusion |
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How does P. Falciparum present?
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Hyperpytexia >106*F
Normocytic anemia because allbeing lysed mimics other diseases such as gastritis. |
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How can you ID P Vivax?
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Do a giemsa stain, look for the diagnostic stages in the erythrocytes (schuffners dots) and know that they are larger then the RBCs around them
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What is often the cause of death in P. Falciparum?
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Kidney damage
High levels of Hgb in the urine and its dark |
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What are the drugs for P. vivax?
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"quines"
Chloroquine quniodine primaquine |
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How is serebral malaria caused with P falciparum?
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The RBCs that are infected are sticky and tend to occlude vessles
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What malaria form is very deatly
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P. falciparum
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What is the incubation for P. falciparum? What cells does it infect?
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8-11 day incubation
invades RBCs of ALL ages so it causes more loss and damage |
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How can one ID P. falciparum?
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Diagnostic stages are seen in erythrocyte.
Look for "double rings" or omc;isopms in RBCs that are the same size as non-infected. sometimes cresent shapped gametocytes are visible |
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How does P. Falciparum present?
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Hyperpytexia >106*F
Normocytic anemia because allbeing lysed mimics other diseases such as gastritis. |
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What are the treatments for P falciparum?
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"quines" and doxycycline and azrythromycin can also be used. Z pack okay in preggers and kids
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What is often the cause of death in P. Falciparum?
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Kidney damage
High levels of Hgb in the urine and its dark |
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How is serebral malaria caused with P falciparum?
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The RBCs that are infected are sticky and tend to occlude vessles
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How can one ID P. falciparum?
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Diagnostic stages are seen in erythrocyte.
Look for "double rings" or omc;isopms in RBCs that are the same size as non-infected. sometimes cresent shapped gametocytes are visible |
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What are the treatments for P falciparum?
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"quines" and doxycycline and azrythromycin can also be used. Z pack okay in preggers and kids
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describe babesia pathology
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Similar to Malaria clinicaly with fever/chills/ha, and destroys RBC
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Where is babesia found and what is the vector?
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New Englanf and deer tick (Ixodes)
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What is the therapy for babesia?
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Clindamycin and quinine
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What are the infective stages for Toxoplasma gondii?
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zoitocyst and oocyst (fromed in cat gut)
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What are the phases of Trophozoites of t. gondii?
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tachyzoite (active merozoite in an acute infection) the bradyzoite (merozoite in the zoitocyst—tissue cyst in chronic disease).
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What do tachyzoites of T. Gondii target?
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Paranchymal cells and the RES
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What is the result of a Toxo infection to fetus?
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CNS disease
Chorioretinits hydrocephaly microcephaly microcephaly stillbirths |
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What is the result of Toxo in an aids patient?
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Possible brain lesion, headache, mental deterioration and chorioretinitis, can also dissminate to other tissues like heart
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How can you get toxo?
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Meat+++Much more likely source
Cat feces transplacental Freezing meat kills cystic stage |
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What form of toxo is in raw meat?
Cat poop? |
Zoitocyst
OOcyst in cat poop |
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Dx stage of Toxo
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tachy and bradyzoites
or do ELISA |
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What is the common name for trypanosoma?
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African sleeping sickness
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How does trypanosomiasis evade detection in the body?
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It has new sureface antigens that it is constantly developing and using
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What is so disgusting about the testefly that infects with african sleeping sickness
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It is a diurnal feeder and poops on you when it eats.
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What si Trypanosoma gambiense?
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CHRONIC African Sleeping sickness
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What are the 4 stages of pathogenicity of T. gambiense?
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Parasitemia
lymphadenitis CNS involvement Trypanosomal chancre (can also see fever, lethargy, paralysus and tongue tremors) |
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What are the resivoirs for T gambiense?
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Humans and pigs
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How do you ID T. gambiense?
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See swirly shaped tropomastigoe in the blood
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What is acute African sleeping sickness? How is it different than gambiense?
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T. rhodesiense
It doesn't hace any somnolence or CNS assocaited with it but it DOES have Encephalomyelitis |
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Which is more deadly, chronic or acute ASS?
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Both deadly but chronic takes years while T. rhodesiences
death usually in less than a year |
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Where is gambiense vs rhodesiences in africa?
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rhodesiences os dry savanna woodlands
gambiense is in humid forests |
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What are the two phases of T cruzi in the body?
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Trypomastigore (blood)
Amastagote (tissue) |
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What is the infective stage of T cruzi and how do you get it?
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Metacyclic is the infective stage from the bug pooping on you and it penetrates the skin. they turn into tropomastagoe->amastagorte and then asexually divide in pseudocysts.
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What disease presents with Romanas sign (swelling of the eyelid) in the acute phase? Who would you see it on?
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Kids <5
It is chagas or T. cruzi |
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What happens in the chronic phase of T Cruzi infection
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This is in adults
chardiac complications Megaesophagus and megacolon. The disease has a preference for cardaic and nervous tissue |
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How is T. Cruzi transmitted? Resivoiur? Vector?
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vector- Triatomid bugs
resivoir- pets and wild animals Transmission- bugs, sex, transfusion, placental and transmammal ( |
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What are the diagnostic stages of T Cruzi
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tropomastigote in the blood, amastigote int he myocardium or xenodiagnosis (looking at the bug that bit)
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is there a vaccine for chagas?
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no
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What is the bug that "kisses" in Chagas?
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Triatomid
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What is unique about Leishmaniasis?
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It is an obligate intracellular parasite
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What is the vector for Leishmaniasis?
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the sand fly
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What is the infective stage of Leishmaniasis? What is the intracellular stage called?
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promastagote
amastagote |
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Describe the pathogenicity or cutaneous Leishmaniasis?
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Ulcer at bite site
amastagoe parasitizes macrophase inflammation results secondary bacterial infections frequent heals spontaneousl in 2m-1 year |
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What form of leishmania is the mucocutaneous form?
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L. brasiliensis
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Describe the pathogenicity of mucocutanteous Leishmaniasis?
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Involves skina nd mucous membranes, cartialge is destroyed
recurrances is possible, resulign in mouth and nose deformities Lesions can be painful with this form (whereas cutanteous was not) |
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What form of leishmania is the visceral form?
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leishmania donovani
aka Kala-azar |
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What is the pathigenisis of Leishmana donovani?
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Skin manifestations and fever, parasite attacks macrophages activating reticuloendothelial cells. Hepatosplenomegaly results
usually not fatal, often asymptomatic |
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What is post Kala-azar?
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the result of inadequate treatemtn of L. donodvani
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What parasitic disease prevents Gulf War vets from donating blood?
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Leishmaniasis
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What schistosomiasis are humans generally infected with?
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S. Haematobium and S. mansoni
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What is Katayama syndrome?
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A early manifestation of schisto that includes nocturnal fever, cougn, myalgia, headache and abdominal tenderness
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What is S. Japonicum and S. manoni known for causing?
|
Granulomas and mildly bloody diarrhea
|
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What is S. Haematobium assocuated with?
|
Bladder cancer and bloody urine
|
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What bactreia is associated with Schisto?
|
Salmonella
|
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What causes the immune response to schisto?
|
The granauloma formation elicited by the eggs in the various viscera
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What cytokines play a role in schisto pathogenicity?
|
IL-7 stimulates worm growth
TNF stimulates egg production |
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How is schisto best detected?
|
Eggs are usually detected in feces or urine, but the longer teh infection goes on, the few eggs there are
|
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What is the DOC for schisto?
|
Praziquantel
|
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What is Cercarial dermatitis?
|
Swimmers Itch- caused byt animal forms os schisto, usually of bird origin
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What is the pathology with swimmers itch?
|
Entrapment of cercariae in the epidemis produces an allergic response
sometimes there is pustule formation with secondary bacterial infections |
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Where is swimmer itch lesions generally seen?
|
Legs
|
|
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What is Dracunculiasis?
|
A large (female) worm that lives in t the skin and sub q tissue that forms painful ulcers and lesions
endemic to aftica |
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What is the infective stage of Dracunculiasis?
|
3rd stage larva (ovoviviparous)
is accidentially eaten when bathing (1st stage eaten by some water dwelling crustation like bug) |
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What is the treatment for Dracunculiasis?
|
As worm emergres to expel larve (usually in fresh water) it should be pulle slowly, each day and wrapped on a stick
There is no effective antihelminth but antibiotics can preent bacteria infection |
|
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What is Wuchereria bancrofti?
|
Filariasis
It causes lymphatic filariasis or lymphedema |
|
|
What is the result of Filariasis?
|
Permanent elephantoid tissue
|
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Describe Filariasis (adults,, morphology and infective stages)
|
• Larvae are microscopic
• Adults are thread-like macroscopic worms • Infective stage—filariform juvenile • Adult worms—reside in lymphatic ducts • Mosquito ingests microfilaria during blood meal |
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What are the vectors for Wuchereria bancrofti (Filariasis)/ Where is the disease found?
|
night-feeding mosquitoes
Africa, Asia, & Brazil |
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What does it meanfor Filariasis to have Microfilarial periodicity?
What is the diagnostic stage? |
peripheral blood w/ maximum number of larvae (10 PM–2 AM)
microfilaria test for it during this time |
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What is the DOC for Filariasis?
|
diethylcarbamazine
|
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What does Brugia malayi or Malayan Filariasis cause?
|
Elephantoid tissue via Mosquito vector
|
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|
What is Onchocerca volvulus commonly called? What is the infective stage?
|
river blindness
filariform larva |
|
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What is the pathology of Onchocerca volvulus? What is the DOC?
|
nodules, elephantoid tissue,
blindness (hence river blindness) ivermectin |
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How is Onchocerca volvulus spread back to vector (and what is it?)
|
Microfilaria is ingested by black fly (Simulium)
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What vector for Onchocerca volvulus? Where does it like to mate?
|
Black fly
Near rapid waters |
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How can you obtain a diagnosis of Onchocerca volvulus?
|
get a tissue sample from one of the nodules and examine
it lives in the skin |
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What is Loaiasis (loa-loa) known to infect? What is the infective stage
|
Flariform larva
affects the EYE and sub q tissue |
|
|
What is the vector for Loa Loa?
|
deer flies
|
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What is the resivoir for Loa Loa?
|
Just Humans
|
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|
What is the treatment for Loa Loa?
|
diethylcarbamazine & surgery
|
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What is Dirofilariasis?
|
Dog heartworm that can also problems in the heart, lung and sub q in humans
|
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|
What is the infective stage for Dirofilariasis? How is it transmitted?
|
filariform larva
Usually from mosquitos to dogs and cyotes |
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|
how is a Dx of Dirofilariasis made?
|
You will see coin lesions on x-ray
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|
A man from Brazil goes to the doctor because of
an enlarge scrotum. A thick blood film reveals microfilariae. Which of the following organisms is the probable causative agent? 1 Leishmania braziliensis 2 Trypanosoma cruzi 3 Loa loa 4 Wuchereria bancrofti 5 Dracunculus medinensis |
4 Wuchereria bancrofti
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|
At an aid station, a 14-yr-old Sudanese rebel
soldier is seen for an infected ulcerating lesion on his leg. A thin worm is clearly visible protruding from the wound. How did he become infected? 1 Mosquito injecting larvae during a blood meal 2 Deer fly injecting larvae during a blood meal 3 Walking barefoot, allowing larvae to enter skin 4 Drinking water that contain infected copepods 5 Swimming in cercariae-infested water |
4 Drinking water that contain infected copepods
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|
The diagnosis of sclerosing keratitis is made in a
patient from Ecuador. Of note are many filariform juveniles in the chambers of the eye. Which of the following parasites is the causative agent? 1Dracunculus medin... 2Toxocara canis 3Loa loa 4Onchocerca volvulus 5Wuchereria bancrofti 0% 0% 0% 0% 0% 1 Dracunculus medinensis 2 Onchocerca volvulus 3 Loa loa 4 Toxocara canis 5 Wuchereria bancrofti |
2 Onchocerca volvulus
|
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What is bacteremia?
|
Presence of bacteria in blood which choulf be sterile
|
|
|
What are the most frequent isolates of bacteremia?
|
Staphylococci and gram negative bacilli
Corynebacterium increasing |
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|
What is the implication of finding s. epidermis, diptheroids, and propionibacteria in the blood?
|
It is generally just a skin contaminant unless >5CFU/ml or repeated cultures is positive
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What is SIRS
|
Systemic inflammatory response syndrome
2 or more of following Fever HR>90 Resp>20 WBS > or < normal range or 10% bands |
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|
What is MODS?
|
Multople ordan dysfunction syndrome. It is when homeostasis cannot be maintained without intervention
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|
What causes SIRS?
|
NOT Microbes
Auto immune, pancratitis, vasculitis, burns, surgery |
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|
What is Spesis
|
it is SIRS + a microbe proven in culture
|
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|
Criteria for severe sepsis
|
Sepsis +1 of signs of hypoprofusion or dysfunction
(mottled skin, capillary refill, uring output decrease, lactace>2, change in mental status, abnormal EEG, platelts <100K, ARDS or acute lung injury, cardaic dysfunction) |
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|
What is septic shock
|
Sepsis definition + at least one of the following
1) systemic arterial<60mmhg despite fluids 2)Drugs are required to maintain BP (even when fluids given) |
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|
What is the difference between 1 and 2ndary MODS?
|
1* is organ dysfunction due to well defined insult
2* is due to a failure of host response impacting organ function |
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|
Three Goals of Septic Shock
|
1) Resucutte patient from shock
2) ID And treat infection 3) Maintian adequate organ system function |
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|
What 2 factors set the stage for infective endocarditis?
|
Drug use and invasive vascular procedures
|
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|
What is the most significant predisposing factor for infective endocarditis? Other causes
|
#1 Residual valvular damage from a previous case of Infective endocarditis
Other factors Rhumatic fever calcific aortic stenosis Congenital heart disease MVP Prosthetic valves |
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|
How does acute IE present? Who is a likely culprit?
|
Abrupt onset
Fever (always) Complications w/in a week - Dyspnea, fatugue, CNS comp Stap aureus |
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How does subacute IE present? Who is a likely culprit?
|
Fever (low grade)
Subtle nonsepcific symptoms (anorexia, weight loss, influenza, ) Onset to dx ~6 weeks Often Viridans streptococci (from imporper abiotc use or immunosupressed) |
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|
What is the current way of classifying IE?
|
By microbe, type and site of valve, and predisposing event
ex: alpha hemolytic streptococcal native valve endocarditis (72%) |
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|
Strep bovis is often seen in Infective endocarditis cases. What lab features ID?
|
Gram +
Gamma Hemolytic Catalase - Group D lancefeild |
|
|
What are the fastedious organisms known for causing subacure endocarditis?
|
Haemophilis aphrophilis
Actinobacillus actinomycetemcomitans Cardiobacterium hominis Eikrnella corrodens Kingella kingae |
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|
What are teh 5 classic signs indicating infective endocardits?
|
Petechiae
subungal hemorrhage Osler nodes Janeway lesions Roth spots |
|
|
What are the 2 steps to form vegitations?
|
Damage to endothelium causea platlet and fibrin aggregation
Organism that is capable to adhering to damaged area seeds there, replicates and causes infectiosu vegitation |
|
|
What are janeway lesions?
|
sign of acute infective endocarditis
Flat, painless, red to bluish red macules on the palms and soles |
|
|
What might splinter petichiae on the nails indicate?
|
Microemboli
|
|
|
What might be seen in the kidney with circulating immune complexes, for example, from a vegitation?
|
Glomerularnephritis and flea-bitten kidney
|
|
|
What are osler nodes?
|
Red painful intradermal transient nodes on the pads of fingers and toes... Pea sized
|
|
|
What are roth spots
|
white ares in the retina that indicate lymphocytes, edema and hemorrhage, seen in IE, but not exclusive to it
|
|
|
What is the consequence of continuous bacteremia?
|
Infectious emboli in brain can lead to stroke
Roth spots and capillary deposition in the hands (janeway lesions) Can also get clubbing or gangrene of the extremities |
|
|
Review Duke Criteria IE
|
Bacteremia Slodes 71-
|
|
|
Morphology of Franciscella tularensis
|
Gram negative, aerobic coccobacillus, FACULTATIVE IC pathogen
|
|
|
How is tularemia spread?
|
Low infectous dose, usually ticks, or animal bite/contact
NO person to person |
|
|
How does tularemia present?
|
Depends on how infected:
Pneumonia if inhalled (with necrotizing granulomas) Skin lesion if bit (Ulceroglandular, MOST common) Oropharyngeal if you ate infected meat systemic spread with typhoidal infection |
|
|
Hat happens if tularemia in the eye?
|
Rare but pain, itching, photophobia, ocular congestion and edema of the conjunctiva
|
|
|
Why is typhoid tularemia difficult to diagnose?
|
No ulcers or lymphadenopathy: patients present wiht fever, wtloss, chills myalgias, often pneumonia though!
|
|
|
How can you make the DX of tularemia?
|
Culture lymph node aspiration
or IgG titer x4, however can have cross rxn with other infections |
|
|
DOC tularemia?
Mortaility rate? |
streptomycin or gentamicin
<1% if treated. 5-30% if not |
|
|
Who is at greatest risk for Brucellosis?
|
People who drink unpasturized milk, and in direct contact with infected animals, lab techs and researchers. most common in Texas and California
|
|
|
B. abortus
|
Brucella from cow
|
|
|
Why is brucella difficult to diagnose?
|
Because it has nonspecific symptoms like non productive coug, feve, chills, etc, however if infection persists abcess and granuloma seen
|
|
|
What is the morphology of Rickettsia?
|
Gram negative bacilli
Obligate Intracellular pathogens that can make own ATP but suck energy from infected host endothelaial cell |
|
|
What are the virulence factors for Rickettsia?
|
Phospholipase D and hemolysin C allows it to survive intracellularly in the host
|
|
|
How sis Rickettsia transmitted?
|
Variesm but all ARTHROPD borne
|
|
|
Describe how Rickettsia infects the cells
|
It attached to endoothelial cell Omp (outer membrane protein) and stimulates PI3K and Cdc42 to activate Arp2/3 which stimulates phagocytosis, however the Phospo D and Hemlysin c allow it to escape and replicate in the cytosol
|
|
|
What are the consequences of Ricksettsia infections?
|
Damage to the endothelial cells infected cause increased vascularpermiabilty and imbalanced fluids/blood
Can lead to encephalitis, pneumonitis and hemorrhagic rash |
|
|
What is most common Ricettsial disease? When and what age group?
|
RMSF - R. rickettsii
Spring/summer kids 5-9 |
|
|
What are the resivoirs and vectors for RMSF?
|
American Dog Tick
Rocky Mountan wood tick Brown dog tick |
|
|
What does it mean to be transovarial? What diesase exhibits this?
|
R. rickettsii (RMSF)
It means that ticks can pass disease on to their young |
|
|
How is RMSF identified on history/exam?
|
Incubates 2-14 days, high fever, severe frontal headache,
2-3 days post fever, a rash on wrists and anlkes then moves inward to trunk and face (RASH NOT SEEN IN ALL PATIETNS) |
|
|
What is mortailty rate R. rickettsii?
|
20-40% start patient ASAP on treatment
|
|
|
What is caused by R. akari? How is it transmitted? (Vector and Resivoir(
|
Rickettsial pox
HOuse mouse and mouse mite are resivoirs, Mouse mite its the vector |
|
|
What does rickettsial pox look like? What is the treatment?
|
A papule develops then ulcerates then scaps. The organism spreads leading to secon phase fever/ha/ and all over pox like rash. tIt is self limited in 2-3 weeks and mortality is 0%
|
|
|
Where is R. conorii found? Who transmitts it?
|
Mediterranean sea and parts of Africa
spread by brown dog tics (that also spreads RMSF) |
|
|
What doe R. conorii cause? How does it appear?
|
Boutonneuse fever/Mediterranean spotted fevere
after 1 week incubation causes high fever, severe HA and usually single simple scab at bite area, progeesses into whole body rash 4-5 days after symptoms appear |
|
|
What causes "American Boutonneuse Fever"?
|
Rickettsia parkeri
seen in east/southeast US |
|
|
how is "American Boutonneuse Fever" spread?
|
Gulf Coast Tick and lone star tick, both are Ambylommas
|
|
|
What are the 4 spotted Fever Rickettsia and what do they cause?
|
R. Rickettsii - RMSF
R. Akari - rickettsialpox R. Conorii - Boutonneuse fever R. Parkeri - american Boutonneuse fever |
|
|
Waht are the three Typus grops of Rickesttsia?
|
R. Prowazekii: Epidemic typus
R. typhi: Murine typhus Orienta tsutsugamushi: scrub typhus |
|
|
What riketsia cause high caises of epidemic typhus worldwide?
|
R. prowazekii
|
|
|
What is the resivor and vector for R. prowazekii? How do you get infected?
|
Res: Human
Vector: Human body louse Transmission: feces scratched into a bite wound. Rarely caused by a bite |
|
|
How does R. prowazekii differ from the RMSF rash?
|
It starts on the trounk and axilla and spreads to the extremities (opposite)
SPARES THE FACE AND ARMS |
|
|
What is Brill-Zinsser disease?
|
It is recrufescent typhus that can occur years after infection with R. prowazekii
|
|
|
Where is R. tyhpi seen? What is resivoir? Vector?
|
Urbacn cities and costal ports in the us, like warm and humid
Resivoir: Rat Vector: Rat flea Tranmission y bite or feces |
|
|
What is reservoir of O. tsutsugamushi?
|
Rodents and mites (transovarial tranmission( and the cector is the Trombiculid mote larvae or Chigger
|
|
|
What does O. tsutsugamushi cause? What rash pattern
|
Scrub typhus
same as others with a papule that ulcerates and becomes scar. after few days rash develops on trunk and spreads centrifugally. |
|
|
What is the causative organism of Ehrlichiosis? MOrphology?
|
Ehrlichia chaffeensis:
gram-negative coccobacillus Cholesterol in membrane; no LPS |
|
|
Geographic distribution Ehrlichiosis?
|
Worldwide; SE and
MW states in US |
|
|
Principle
reservoi rEhrlichiosis? |
Horses, deer, dogs,
ticks |
|
|
Principle
vector Ehrlichiosis? |
Lone-star tick
|
|
|
Clinical
manifestations Ehrlichiosis? |
Infects monocytes/
macrophages; Non- specific symptoms; rash present in ~20% of pts |
|
|
Mortality rates Ehrlichiosis?
|
2-3%
|
|
|
Treatment Ehrlichiosis?
|
Doxycycline - initiate tx upon suspicion
|
|
|
Causative organism Anaplasmosis? Morphology
|
Anaplasma
phagocytophilum: gram- negative coccobacillus Cholesterol in membrane; no LPS |
|
|
Geographic distribution Anaplasmosis?
|
Worldwide; MW and NE
states in US |
|
|
Resivoir of Anaplasmosis ?
|
Various small mammals
|
|
|
Vector of Anaplasmosis?
|
Black-legged ticks
|
|
|
Clinical Manifestations of Anaplasmosis
|
Infects neutrophils;
similar symptoms as ehrlichiosis; rash present in ~10% of pts |
|
|
Mortalitly rate Anaplasmosis
|
<1%
|
|
|
Treatment Anaplasmosis
|
Doxycycline - initiate tx
upon suspicion |
|
|
Causative agent Q fever? Morphology
|
Coxiella burnetii: gram-
negative bacillus |
|
|
Geographic distribution Q fever?
|
Worldwide; uncommon
in US |
|
|
Resivoir Q fever?
|
Many animals, birds,
and ticks |
|
|
Vector Q fever?
|
Humans: no vector.
Transmission: inhalation (common) |
|
|
Clinical manifestations Q fever?
|
Initial proliferation in
lung macrophages. Acute: asymptomatic or mild – can mimic atypical pneumonia and cause hepatitis; Chronic: subacute endocarditis |
|
|
Mortailty Q fever?
|
Acute: ~1%
Chronic: ~65% |
|
|
Treatment Q fever?
|
Acute: Doxycycline
Chronic: Combination |
|
|
Other info about the makeup of Q fever?
|
Weak LPS activity;
antigenic variation (phase I and II). Serology indicates patient status. |
|
|
How does Salmonella Typhi grow
|
Gram- on regular medium
non lactose ferment Produces H2S black colonies on hektoen ENteric agar and clear colonies on MacConkeys |
|
|
What does hektoen Enteric agar select for?
|
Samonella shigella and other enterics
it also differentiaats lactose (e-coli) from other non lactose fermenters |
|
|
What are the virulence factors of Salmonella typhi? What cells does it attack?
|
It is an intracellular parasite in macrophages
Its invasive and associated with Type 3 secretory system (bacteria endocytosis, cell rubbling and m csells and enterocytes) |
|
|
What are the 6 major pathogeniicty factors of salmonella?
|
O-antigen
H-antigen LPS - Lipid A And Pathogenicity Islands Vi (Virulence antigen) capsule |
|
|
What are patients with achlorhydria more susceptible to?
|
infections with S. typhi
|
|
|
What pathogen proliferates in peyers patches?
|
S Typhi
|
