Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
282 Cards in this Set
- Front
- Back
|
If you see a Downey Cell, what is it?
|
IM caused by EBV
|
|
|
What are the complications of EBV?
|
Rash after penicillin
Splenic rupture (rare Chronic Disease Malignancies - Post-Transplant lymphoproliferative Disease, Burkitts Lymphoma, Non-Hodgkin's lymphoma, Hodkin's Disease, Nasopharygeal carcinoma (China) |
|
|
How do you diagnose CMV?
|
Serology (ELISA testing for CMV specific IgM antibody) is good and the most common way to reveal a primary infection or reaction.
|
|
|
How does HIV attach to a host cell?
|
Interactions with host receptors (gp120 attaches to CD4. CD4-gp120 complex attaches to coreceptor)
Fusion of the envelopes (gp41) Insertion of capsid into cytoplasm (uncoating capsid relseases viral RNA and gag and pol proteins |
|
|
If a patient shows signs and symptoms of IM, but serology is negative for heterophile antibodies and EBV-specific antibodies, you then then suspect….
|
CMV first, but check for HIV as well
|
|
|
If a patient shows sugns and symptoms of hepatitis, but is negative for hep A, B and C antigens or antibodies, you should suspect…
|
CMV
|
|
|
What is the most common infection of the fetus and a major cause of morbidity/mortality in HIV and transplant patients?
|
CMV
|
|
|
What is the hallmark of EBV infection?
|
polyclonal proliferation and activation of B-cells
|
|
|
Which infection or virus below is INCORRECTLY matched with its virus class?
A. EBV - gamma herpesvirus B. CMV - beta herpesvirus C. mumps - paramyxovirus D. HepA - hepadnavirus E. HepC - flavivirus |
D. HepA is a picornavirus. HepB is a hepadnavirus
|
|
|
Which infections pass through the placenta?
|
ToRCH
Toxoplasmosis Rubella Cytomegalo virus Herpes simplex |
|
|
Who gets CMV infections?
Who gets CMV disease? |
80% of population is infected with CMV at some point in their life.
Only immunocompromised develop disease from the infections - infants, elderly, HIV, transplant patients, etc. |
|
|
a 17-25 yr old patient presents with sore throat, bilateral lymphadenopathy, fever, hepatosplenomegaly, and palatal erythema w/ petechia.
What is the most likely diagnosis? How do you confirm diagnosis? If most likely diagnosis is proved wrong, what else should be considered? |
Most likely has IM from EBV infection
If confirmed, blood will show atypical lymphocytes in circulation and heterophile antibodies will agglutinate horseblood on a MONOSPOT TEST due to Paul Bunnell antigen on animal erythrocytes. (if pediatric case, use VCA (virus capsid antigen) test instead since heterophile ab is not reliable in that population). If EBV is not confirmed, then test for CMV (next most likely) and HIV. |
|
|
What is the relationship between EBV and Burkitt's lymphoma?
|
EBV infection is probably contributory, but nonessential cofactor for malignancy
|
|
|
What is the basic lesion of Burkitt's Lymphoma is caused by?
|
dys-regulation of c-myc,
|
|
|
What produces a characteristic CPE with gross enlargement and intranuclear and intracytoplsmic inclusions and fused syncytica
|
CMV
|
|
|
patients with abnormal atypical lymphocytes that are heterophile antibody negative, have what?
|
Heterophile AB negative = CMV
|
|
|
Fetuses infected with CMV in utero are at risk for?
|
permanent brain damage
|
|
|
An estimated 25% of AIDS patients develop some form of CMV disease, How does this manifest?
|
Retinitis
GI disorders CNS disease Pneumonias |
|
|
If you see a greatly enlarged (cytomegalic) cell with characteristic “owl eye” nuclear inclusion body, then the patient has…
|
CMV infection
|
|
|
Treat CMV with
|
Ganciclovir
Foscarnet Fomivirisen Immunoglobulin for persons with severe disease |
|
|
Linear ssRNA genome, (-) sense, approximately 16 kb in size
Helical nucleocapsid Enveloped, virions exhibit a highly pleomorphic shape Virus has spikes with combined hemagglutinin and neuraminidase activities What is it? |
paramyxovirus (causes mumps)
|
|
|
What are the clinical manifestations of mumps?
|
• Acute infection of the salivary glands with associated painful swelling and fever
• High fever, vomiting, headache • Rapid onset • Virus will spread to other organs • Many mumps infections are asymptomatic (30%) • 30% of adult males will develop orchitis |
|
|
How is mumps spread?
|
Person to Person
Transmission by aerosols highly communicable infection |
|
|
How is CMV spread?
|
person to person
any bodily fluids (saliva, urine, blood, mucuos, sexual contact, and DONOR ORGANS) |
|
|
How is EBV spread?
|
Person-to-person transmission via droplets/contact (especially saliva)
"Kissing disease" Considered to be of relatively low contagiousness, BUT virus can sustain in saliva long after symptoms regress |
|
|
What are the comllications associated with mumps?
|
deafness (children), orchitis, oophoritis, mastitis, pancreatitis, spontaneous abortion
|
|
|
how do you treat mumps?
|
symptomatic releif
|
|
|
Which component of MMR vaccine has lowest efficacy?
A. Measles B. Mumps C. Rubella |
B. Mumps.
perhaps 10% of total recipients remaining unprotected after two administrations 1996 outbreak suggests third administration may be beneficial |
|
|
Which viruses are characterized by positively-stranded, enveloped ssRNA, an envelope containing viral glycoproteins, viral enzymes within the capsid, latency after integration into host DNA, and virion release via budding from host plasma membrane?
|
Retroviruses (HIV and HTLV)
|
|
|
What are some important general characterisitics about retroviruses?
|
1. Positively-stranded, enveloped ssRNA diploid viruses. The envelope contains viral glycoproteins.
2. Within the capsid are viral enzymes, including reverse transcriptase and integrase. 3. The viruses gain access to host cells by interaction with receptors on host cells, fusion of the envelope, and insertion of the capsid into the cytoplasm. 4. The RNA is copied into DNA by the enzyme reverse transcriptase, and the viral DNA then integrates into the host genome and remains latent for a period of time. 5. When stimulated, many virions are produced and are released by budding from the plasma membrane. |
|
|
Which HIV genome encodes a precursor that is cleaved into four functional nucleocapsid proteins: p7, p9, p17, and p24?
|
GAG
|
|
|
Which HIV genome encodes a precursor that is cleaved into viral enzymes: protease (p10), reverse transcriptase (p51, p64), and integrase (p32)?
|
POL
|
|
|
Which HIV genome encodes a precursor that is cleaved into two envelope glycoproteins gp41 and gp120, allowing viral attachment and fusion to CD4 cells?
|
ENV
|
|
|
viral proteins p51 and p64 make…
|
reverse transcriptase
|
|
|
viral protein p10 makes?
|
protease
|
|
|
integrase is made of which viral protein?
|
p32
|
|
|
Which viral protein is INCORRECTLY matched with its HIV genome?
A. p10 - POL B. p51 - POL C. gp120 - ENV D. p17 - GAG E. p24 - POL |
E. p24 is on GAG
POL has p10 (protease), p51 & p64 (reverse transcriptase) and p32 (integrase) ENV has the glycoproteins gp41 and gp120 GAG has four functional nucleocapsid proteins, p7, p9, p17 and p24 but she didn't tell us what their functions were so if they are in a question then they're likely distractors |
|
|
what does gp120 do?
|
attaches to host receptor CD4 to help HIV-1 attach to host cell
|
|
|
What does the HIV enzyme integrase do and what protein is it?
|
incorporates the DNA randomly into the host genome. P32
|
|
|
What does the HIV enzyme protease do and what protein is it?
|
cleaves the polypeptide chain into some of the functional proteins. After release, cleaves the remaining polypeptide, forming the functional reverse transcriptase & core proteins. P10
|
|
|
How many core proteins are their in an HIV virus?
|
Nine. We're only responsible for three (gag, pol, and env)
|
|
|
what are the four stages in the progression from HIV infection to AIDS.
|
1. Acute HIV infection
2. Clinical latency: 3. Early symptomatic HIV infection 4. AIDS |
|
|
How does one make a diagnosis of AIDS?
|
Defined by the CDC as being HIV positive and presenting with 1+ of the 26 AIDS defining opportunistic infections or malignancies
OR having a CD4 T count below 200 cells/microlitre OR having CD4 T cell % below 14. |
|
|
How does AIDS-related dementia develop?
|
macrophages can deliver HIV to the microglia and neurons, causing deterioration
|
|
|
How does acute HIV infection usually present?
|
May be asymptomatic, but is symptomes are present they resemble flu or IM: fever, runny nose, sore throat, exhaustion, and a rash.
|
|
|
what causes the symptoms of acute HIV infection?
|
production and release of cytokines from infected CD4 cells and macrophages
|
|
|
An HIV positive patient presents with chronic symptoms of lymphadenopathy, weight loss, malaise, fever, diarrhea, and night sweats. What stage of disease is he likely in?
|
3. Early symptomatic HIV infection
|
|
|
What antibodies are diagnostic of HIV?
|
anti-gp120
|
|
|
When testing suspected HIV patients blood with Western Blot, what are the generally accepted banding patterns that confirm HIV?
|
p31/32 OR p24
AND gp160/120 OR gp41. |
|
|
How is PCR used with HIV patients?
|
assesses viral load
can be used for diagnosis, but often used to monitor effectiveness of drug therapy. "My T-cells are low. I regret that news." = PCR monitoring |
|
|
regarding HIV, what does HAART stand for?
|
Highly Active Anti-Retroviral Therapy
|
|
|
What are the seven classes of HAART drugs?
|
1. Nucleoside analogs: include Retrovir® (zidovudine, AZT), Videx® (didanosine, ddI), Hivid® (zalcitabine, ddC), Zerit® (stavudine, d4T) and Epivir® (lamivudine, 3TC).
2. Non-nucleoside analogs: include Viramune® (nevirapine) and Rescriptor® (delavirdine) 3. Protease inhibitors: include Invirase® (saquinavir), Norvir® (ritonavir), Crixivan® (indinavir), and Viracept® (nelfinavir). 4. Entry/fusion inhibitors: include Fuzeon® (enfuvirtide) and Selzentry® (maraviroc). Others in clinical trials (such as PRO 140 and ibalizumab) 5. Integrase inhibitors: include Isentress® (raltegravir) and others currently in clinical trials. 6. Maturation inhibitors: PA-457 (bevirimat) and MPC-9055 (vivecon) are in clinical trials. 7. Antisense “drugs”: HGTV43 is a retroviral vector encoding HIV antisense genes. |
|
|
How is HIV/AIDS treated?
|
combination of HAART drugs (types change throughout therapy and are adjusted according to stage of illness and patient responsiveness) as well as specific treatment regimes for opportunistic infections
|
|
|
What are the two genera of Retroviruses that infect humans and cause disease?
|
Lentiviruses (HIV1 and HIV2)
Oncoviruses (HTLV-1 and HTLV-2) |
|
|
Are oncoviruses cytolytic?
|
No.
|
|
|
What is similar about HIV and HTLV?
What is different about them? Looking for Big Picture here |
Similar: retroviruses; attack t-cells; incorporate into DNA; establish latency; develop into incurable disease
Different: HIV is cytolytic and will diminish t-cell count until AIDS develops. Will also infect macrophases and monocytes which release cytokines and help virus spread faster. HTLV is not cytolytic and may not progress to ATLL or may not; ATLL causes a malignant proliferation of CD4+ T cells. |
|
|
what are the clinical manifestations of acute T-cell lymphocytic leukemia (ATLL)?
|
Malignant proliferation of CD4+ T cells is seen. This results in generalized lymphadenopathy, hepatosplenomegaly, and widespread cutaneous papulonodular lesions.
|
|
|
What complications are seen with ATLL?
|
infections with opportunistic pathogens, such as PCP, fungal infections, and herpesvirus infections as well as tropical spastic paraparesis (bilateral progressive weakness of lower limbs with some stiffness, some sensory loss, and possible hyperactive reflexes)
|
|
|
What HTLV gene transactivates the genes for IL-2 and IL-2R.
|
tax
|
|
|
IL-2 and IL-2R are normally produced by ______________________
Production of IL-2 and IL-2R without antigen stimulation results in _______________________________ |
the T cell upon antigen stimulation.
uncontrolled clonal proliferation. |
|
|
In the U.S., what is the most common mode of transmission of HTLV?
|
IVDU and blood transfusion
but can also be acquired by sexual contact (including artificial insemination). |
|
|
How do you diagnose HTLV?
|
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. |
|
|
How do you treat HTLV/ATLL
|
Lymphoma chemotherapy
Combination of IFN-α and AZT |
|
|
What is the latency period for HTLV?
|
30-50 years
|
|
|
What is the pathogenesis of HIV?
|
Destruction of helper T cells; cytokine stimulation enhances HIV replication
|
|
|
What is the pathogensis of HTLV?
|
Uncontrolled proliferation of helper T cells; transactivation of IL-2 and IL-2R
|
|
|
How does HepA differ from other picornaviruses?
|
Mature virions are released by exocytosis, NOT cell lysis as other picornaviruses.
|
|
|
A patient has severe symptoms of acute viral hepatitis and is admitted to hopsital for treatment and monitoring. Serology confirms HepA infection. He is worried that he might infect his family if they visit him. None of them currently show any symptoms.
What signs is he likely showing? What complication are you monitoring for? What do you tell him about his family visiting? What can you give his family members? |
Clinical signs: Early symptoms are fever, fatigue, nausea, loss of appetite, and abdominal pain. Later, symptoms can also include jaundice, icterus, dark urine, and colorless stool.
Complications: You're really not worries about anything. Mostly just treating symptoms to keep the patient hydrated and comfortable. Fulminant hepatits is extremely rare with HepA but possible (<1%). Transmission: HAV is shed in the stool 2-3 weeks prior to onset of symptoms and most infectious during that period. It usually takes 2-6 weeks to develop into disease once you're exposed, so anyone patient has been in close contact with may have already been infected, even if they're not showing signs. Children under 6 yo may never develop symptoms. Teens and adults who have been infected probably will show symptoms. Either way, visiting him at this point should not increase their risk. Treatment/Prevention: Post-exposure prophylaxis with immune globulin might be a very good option to give his family to prevent or minimize symptoms. |
|
|
What causes the jaundince and colorless stools associated with viral hepatitis
|
occur as a result of liver damage; bilirubin cannot be taken up from the plasma at a high enough rate and therefore concentrates in the tissues. The lack of bilirubin in the bile results in the colorless stools.
|
|
|
Why is HepA virus least likely to cause chronic problems?
|
Virus doesn't lyse cells. Releases via exocytosis. So the virus itself does not cause lasting liver damage.
The liver damage that occurs with HepA infections comes from the bodies immune response when CTL (cytotoxic T lymphocytes) and ADCC (antibody dependent cellular cytotoxicity) try to eliminate the virus. |
|
|
Who is at highest risk of mortality with HepE infection?
|
pregnant women
|
|
|
Which viral hepatitis does this describe? A small, enveloped, partial-stranded DNA virus, called the Dane particle. It is unusually stable.
|
the Hepadnavirus of HepB
|
|
|
Chronic HepB infection occurs if…
|
If CMI/inflammatory responses are inadequate
|
|
|
What age group is most likely to contract acute HepB infection?
What age group is most likely to see an acute HepB infection progress to chronic HepB? |
Highest rate of disease in 20-49 age class.
young children often become chronic HBV carriers. |
|
|
Which viral hepatitis has two envelope glycoproteins (E1 and E2) which bind CD81 on hepatocytes?
|
HepC
|
|
|
Which viral hepatitis is a flavivirus?
|
HepC
|
|
|
Which viral hepatitis is a picornavirus?
|
HepA
|
|
|
Which viral hepatitis is a hepadnavirus?
|
HepB
|
|
|
Which viral hepatitis is a hepevirus?
|
HepE. Duh. "HepEvirus"
|
|
|
Which viral hepatitis can incorporate itself into host hepatocyte DNA?
|
HepB, a "HepaDNAvirus"
|
|
|
Which statement is true about HBs-antibodies?
A. They are only found in people who have had HepB vaccination. B. They are found in everyone who has recovered from viral hepatitis. C. Only protect people from getting HepB infection. D. Attack HepB and HepD viruses. E. Indicate person may be susceptible to HepB infection. |
D. Hepatitis B surface antibodies attack HBs-antigens, which are found on the envelope of both HBV and HDV.
|
|
|
What is the most common HCV genotype in the US?
|
Genotype 1 (subtypes 1a and 1b). Accounts for 70% of US HCV infections
|
|
|
How is HCV transmitted?
|
exposure to infected blood. (High-risk groups: transplant/transfusion patients, IVDU/intranasal cocaine use, and sexual contact with infected persons.)
|
|
|
What is the most common cause of chronic hepatitis and subsequent need for liver transplantation?
|
HCV
|
|
|
Who have cause for a strong suspicion of HCV infection, but there are no HCV antibodies found in your patient's blood. What else can you do to confirm HCV diagnosis?
|
test for HCV RNA in blood of seronegative patients
|
|
|
which viral hepatitis can be transmitted perinatally?
|
HBV
|
|
|
Which viral hepatitises cannot be prevented with vaccines?
|
HCV and HEV. HBV vaccine prevents HDV as well.
|
|
|
Interferon-alfa, ribavirin, NS3/4A protease inhibitors are all common drug treatments for which viral hepatitis?
|
HCV
|
|
|
Which viral family is matched INCORRECTLY with one of its VHF viruses?
A. Filoviridae: Marburg B. Bunyaviridae: Hantaan C. Arenaviridae: Ebola D. Flaviviridae: Dengue |
C. Ebola is a Filovirus, like Marburg.
The VHF arenaviridae we learned about is Lassa |
|
|
Which statement about VHF's is INCORRECT?
A. All are enveloped RNA viruses. B. The true reservoir of each virus is an animal or insect. C. They are geographically restricted to the areas where their host species live. D. Transmission only occurs via an arthropod vector or contact with rodent excretions |
D. While the viruses are generally transmitted via arthropod vector or rodent excretions, human-to-human transmission can occur for a few of these viruses once a person becomes infected.
|
|
|
What are the common clinical symptoms associated with all VHFs?
|
fever, hemorrhagic manifestations, thrombocytopenia, shock, and neurological disturbances.
|
|
|
What causes the fever and hemorragic manifestations in VHF
|
Virus initially infects tissue macrophages and dendritic cells. Infection leads to the release of cytokines – these cytokines stimulate inflammatory processes and activation of clotting pathways
|
|
|
Why to VHF's show descreased immune responses?
|
infection of dendritic cells reduces expression of costimulatory molecules, leading to decreased immune responses.
|
|
|
Dengue virus can cause Dengue Hemorragic Fever (DHF) and Dengue Fever (DF). DHF has a 50% mortality rate if left untreated and 3% if it is treated, while DF has a mortality rate close to 0%. What determines whether a patient gets DF or the deadlier DHF?
|
Prior infection of DF.
Development of DHF requires sensitization of immune systom due to a prior DF. Therefore, if you've never had DF and you get infected with one of the four strains of dengue virus, then you only get DF. After that, you're immune to the strain that infected you, but if you then get infected by one of the three other strains, your immune system promotes the uptake of the virus without neutralizing it, so you get DHF. |
|
|
Natural resevoir for Dengue?
|
Primate. Mostly monkeys
|
|
|
vector for Dengue?
|
Aedes aegypti mosquito
|
|
|
locations of Dengue?
|
several: India, Japan, West Africa, eastern Mediterranean, SE Asia, Indonesia, NE Australia, Polynesia, Caribbean, S. America, and Mexico.
|
|
|
how long does dengue fever last?
|
two weeks
|
|
|
Student doctor leaves the US for the first time to go on a medical mission to Central America. He is bitten by the Aedes aegypti mosquito and develops an infection from it. Describe the symptoms he will develop, course of the disease and any possible treatment options.
|
Patient has dengue fever. He will have an acute infection (2-8 day incubation) characterized by high fever, prostration, headache, anorexia, myalgia, lymphadenopathy, and leukopenia. During the first 1-2 days of symptoms, a rash develops, fades, and then, within a few days after that, a secondary maculopapular rash on the limbs/face with desquamation is seen. The disease resolves within two weeks due to immune clearance of the virus.
Only treatment options are symptomatic relief. |
|
|
Jaundice, black vomit, and Councilman bodies are distinct for which VHF?
|
Yellow fever.
|
|
|
Which VHF's are associated with Central and South America?
|
Dengue and Yellow Fever
|
|
|
Which VHF's are flaviviruses?
|
Dengue and Yellow Fever
|
|
|
Which VHF is more common in children than adults?
|
DHF
|
|
|
The Striped field mouse is the natural resevoir for which VHF?
|
Hantaan virus
|
|
|
Which three VHF's are bunyaviridae?
|
Rift valley fever, hantaan virus, and Crimean-Congo hemorrhagic fever virus
|
|
|
which VHF occurs primarily in Asia and Europe?
|
Hantaan virus
|
|
|
Which VHF is found in livestock and can cause blindness in humans?
|
Rift Valley Fever
|
|
|
Which bunyavirus presents similarly to Dengue fever?
|
Crimean-Congo
|
|
|
blindness is a potential complication of which VHFs?
|
RVF and Hantaan
|
|
|
Which VHF virus has a sandy appearance due to the presence of host ribosomes within the envelope?
|
Lassa virus
|
|
|
Which VHF virus is a large (~120 nm), circular, enveloped ssRNA virus with a negative sense L strand an ambisense S strand?
|
Lassa virus
|
|
|
Where is Lassa virus primarily found?
|
West Africa
|
|
|
which VHF viruses can be transmitted person-to-person by close contact with infected individual?
|
Lassa virus (probably Ebola and Marburg as well)
|
|
|
one third of Lassa fever survivors report what complication?
|
hearing loss
|
|
|
fruit bats are a natural resevoir for which VHF virus?
|
Marburg
|
|
|
which VHF virus has a vaccine?
|
Yellow fever.
|
|
|
Which VHF virus is endemic to Africa, has no known natural resevoir or vector, causes rapid, extensive tissue necrosis and is particularly deadly if contracted in Zaire?
|
Ebola
|
|
|
Ribavirin has been shown to reduce morbidity and mortality rates for which VHF viruses?
|
Lassa, Hantaan, and Rift Valley fever
|
|
|
VHF's that are NOT arboviruses?
|
Lassa, Hantaan, Ebola, Marburg
|
|
|
VHF's with mosquito vector?
|
Dengue, Yellow Fever, Rift Valley fever
|
|
|
VHF associated with tick vector?
|
Crimean-Congo
|
|
|
Memorize all the stages of malaria life cycle found in the human
|
sporozoites, trophozoites, schizont, merozoite, gametocyte
|
|
|
what stage are malaria in when injected into bloodstream via mosquito bite? (infective stage)
|
Sporozoites
|
|
|
which human stage of malaria is NOT found in the RBC?
|
sporozoites
|
|
|
which stages of malaria are ONLY found in the mosquito?
|
zygote, ookinete, oocyte
|
|
|
which stage of malaria is transferred to the mosquito from the human?
|
gametocyte
|
|
|
which stage is malaria in when it invades human RBCs?
|
merozoites
|
|
|
what development stage is malaria in when it forms the "ring stage"
|
trophozoite
|
|
|
Where does asexual division occur for plasmodium vivax?
|
human liver. This is the schizont phase
|
|
|
where does sexual fertalization occur for plasmodium falciparum?
|
In the mosquito
|
|
|
List the plasmodium life cycle stages in chronological order starting with mosquito insertion into human bloodstream.
|
Sporozoite -> EE schizont -> EE merozoite -> young trophozoite (ring or signet form) -> older trophozoite (ameboid and schizont forms) -> RBC schizont (segmenters) -> RBC merezoite -> gametocyte (micro or macro) -> mosquito ingests gametocyte -> fertilization produces gamete - ookinete -> oocyst -> sporocytes
|
|
|
why are many african americans and west africans resistant to plasmodium vivax?
|
Lack Duffy antigen
|
|
|
why are many african americans and west africans resistant to plasmodium falciparum?
|
sickle cell
protozoan has difficulty utilizing the abnormal hemoglobin |
|
|
is malaria caused by a virus?
|
no. Plasmodium spp are protozoans
|
|
|
vector for malaria?
|
night-feeding anopheline mosquito.
|
|
|
Lab reports enlarged infected RBC with Schüffner's dots (stippling; surface invaginations). What is it?
|
plasmodium vivax
|
|
|
Plasmodium vivax causes what kind of malaria?
|
Benign Tertian Malaria
|
|
|
Plasmodium falciparum causes what kind of malaria?
|
Malignant Tertian Malaria
|
|
|
which plasmodium life cycle stage is manifested as fever and chills in the patient with malaria?
|
rupture of RBC schizonts.
|
|
|
In malaria, what inflammatory response causes hypothalamus to raise body temp set point?
|
pyrogen
|
|
|
what receptor does merozoite attach to on RBC?
|
Duffy antigen
|
|
|
what is different clinically from plasmodium vivax and plasmodium falciparum?
|
Falciparum is extremely virulent, has higher fever (>106F), less pronounced chills, may develop "blackwater fever" from hemoglobin in urine, and is often fatal. No recurrent infections.
Vivax is less virulent (only infects young RBCs), lower fever, more pronounced chills, no blackwater urine, is rarely fatal. Also, may develop recurrent infection. |
|
|
occlusion of the capillaries with parasitized RBCs that result in necrosis (possibly hemorrhages), fever >108°F mania, convulsions and death.
|
cerebral malaria
associated with plasmodium falciparum |
|
|
what causes Nantucket Island Fever?
|
aka babesiosa
caused by babesia microti |
|
|
If you see a patient in the northeastern US with malaria-like symptoms, but has never left the country, what does he likely have and what should you look for to confirm?
|
likely babesiosis. Look for a tick bite
|
|
|
If you see a Maltese cross formed in a RBC what are you looking at?
|
Troph stage of babesiosis.
|
|
|
infective stage of toxoplasma gondii?
|
zoitocyst (in meat) or oocyst (in cat feces)
|
|
|
who should be concerned about toxoplasmosis?
|
HIV patients and women who are pregnant or trying to get pregnant
|
|
|
what may happen to fetus if pregnant women gets toxoplasma gondii infection early in her pregnancy?
|
CNS disease, chorioretinitis, hydrocephaly, microcephaly, stillbirths
|
|
|
what happens to AIDS patients infected with toxoplasma gondii?
|
Focal brain lesions, Headaches, Mental deterioration, Chorioretinitis, cysts in muscle (including heart)
|
|
|
what are the modes of transmission for toxoplasma gondii?
|
ingesting infected meat (most common), ingesting cat feces, transplacentally
|
|
|
how do you prevent toxoplasma gondii infection from meat?
|
Cook it throughly and freeze it solid
|
|
|
Diagnostic stage of toxoplasma gondii?
|
tachyzoite & bradyzoite
|
|
|
treatment for toxoplasma gondii?
|
• DOC—pyrimethamine + sulfadiazine
• Alternative—spiramycin |
|
|
what are the causative agents of African sleeping sickness?
|
trypanosoma brucei gambiense (West Africa)
trypanosoma brucei rhodesiense (East Africa) |
|
|
vector for T. brucei gambiense?
|
tsetse fly
|
|
|
patient recently returned from West Africa mission trip and presents to clinic with cc of chronic fatigue. He has fever and lymphadenopathy. Physical exam reveals chancre at base of neck.
Most likely diagnosis? How do you confirm? |
African Sleeping Sickness from trypanosoma brucei gambiense
Confirmed by Trypomastigote in blood smear |
|
|
resevoir for T. brucei gambiense?
|
pigs and people
|
|
|
resevoir for T. brucei rhodesiense?
|
game animal
|
|
|
prognosis for acute african sleeping sickness?
|
dead in < 1 year
|
|
|
Sometimes referred to as American trypanosomiasis?
Causative agent? Endemic area? |
Chagas
Trypanosoma cruzi. mostly in rural and impoverished regions of Latin America. |
|
|
Infective stage of Trypanosoma cruzi?
Vector? |
metacyclic trypomastigote.
Reduviid bug |
|
|
How does the Reduviid bug infect people?
|
Likes to bite, but t. cruzi is not transmitted that way.
droppings (poop) left on skin while it feeds get into bite wound |
|
|
how does reduviid bug get t. cruzi?
|
ingest trypomastigotes from biting infected person
|
|
|
who gets acute phase chagas?
|
children under 5
|
|
|
who gets chronic chagas?
|
adults
|
|
|
what is Romana's sign and what is it characteristic of?
|
It is a swelling of the eyelid as a result of accidentally rubbing bug feces into the eye
occurs in about 50% of the patients with acute Chagas (t. cruzi) |
|
|
diagnositc stages of T. cruzi?
|
trypomastigote (blood) and amastigote (pseudocysts)
|
|
|
An middle aged Latin American with megacolon likely has?
|
chronic chagas
|
|
|
how is t. cruzi transmitted?
|
Lots of ways!
(1) Arboborne. (2) Venereal (transmitted during sexual intercourse). (3) Blood transfusion and organ transplantation. (4) Transplacental (ie, to the fetus across the placenta). (5) Transmammary. |
|
|
why is chronic Chagas difficult to diagnose.
|
may be asymptomatic for years.
T. cruzi amastigote migrates to muscle tissue (cardiac complications) and nerve tissue (ganglion damage = megacolon and mega esophagus) so it does not show on blood smears. |
|
|
Leishmaniasis vector?
|
sand fly
|
|
|
infective stage of Leishmaniasis?
|
promastigote in droppings of sand fly get into bite wound
|
|
|
most likely life cylce stage of Leishmaniasis found in human host?
|
intracellular amastigote
|
|
|
infection from L tropica, L mexicana or L braziliensis will give you?
|
cutaneous leishmaniasis (disgusting skin ulcers at bite site. May develop secondary infections)
|
|
|
Mucocutaneous Leishmaniasis is only contracted from?
|
L. braziliensis
|
|
|
clinical signs of mucocutaneous leishmaniasis?
|
Painful mouth & nose deformities due to destruction/necrosis of skin, mucous membranes and cartilage. Recurrence and secondary infections are possible.
|
|
|
Visceral Leishmaniasis is caused by?
|
Leishmania donovani
|
|
|
Sometimes known as kala-azar
|
visceral leishmaniasis
|
|
|
What is a Leishman-Donovan body?
|
amastigote of leishmania spp
|
|
|
clinical manifestations of visceral leishmaniasis?
|
high fever, hepatosplenomegaly, lymphadenopathy, Splenomegaly
|
|
|
Causative agent of cutaneous leishmaniasis in Africa?
|
Leishmania tropica
|
|
|
Causative agent of cutaneous leishmaniasis in the Middle East?
|
Leishmania tropica
|
|
|
where are you if you get mucocutaneous leishmania
|
Latin America.
L. braziliensis is only causative agent |
|
|
What type of leishmaniasis might you get if you are bit by a sand fly in the Middle East?
|
Cutaneous (L. tropica) or Visceral (L donovani)
|
|
|
What is the treatment for leishmaniasis?
What is a possible result of not treating visceral leishmaniasis? |
DOC: stibogluconate sodium.
Post-kala-azar is a result of inadequate treatment. |
|
|
responsible for the disease manifestations associated with blood flukes?
|
eggs trapped in tissue
|
|
|
which schistosome has zoonotic resevoir?
|
S. japonicum
|
|
|
which schistosomes are primarily human parasites
|
S. haematobium and S. mansoni
|
|
|
which schistosome is associted with bladder carcinoma?
|
S. haematobium
|
|
|
which schistosome is found is Central and South America?
|
S. mansoni
also found in Afric and Middle East |
|
|
Schistosome infection in Middle east that causes GI problems?
|
S.mansoni.
If GU problems then S. haematobium |
|
|
Schistosome infection in the Far East will most likel present with what manifestations?
|
nocturnal fever, cough, myalgia, headache, abdominal tenderness and chronic, mild bloody diarrhea. Chronic will cause fibrosis in liver and intestine
|
|
|
Infective stage of schistosome?
|
cercariae
|
|
|
which schistosome species cause Katayama Syndrome?
|
Any. This is a hypersensitive reaction that can occur during the migratory phase of infection. Clinical manifestations are nocturnal fever, cough, myalgia, headache, abdominal tenderness
|
|
|
which schistosome is most associated with Hepatic fibrosis and portal hypertension?
|
S. mansoni
|
|
|
what bacterial infection is associated with all schistosome infections?
|
Salmonella
|
|
|
how do you confirm diagnosis of schistosome infection?
|
eggs in urine (s. haematobium) or feces (s. mansoni and s. japonicum)
|
|
|
what causes cercarial dermatitis (“swimmer’s itch”)?
|
bird schistosomes
|
|
|
treatment for schistosomiasis?
|
DOC is praziquantel
|
|
|
clinical manifestations of cercarial dermatitis are caused by….
|
allergic reaction to entrapped cercariae in epidermis
|
|
|
the worm that gets pulled out of the skin by slowly winding it on a stick is called?
|
Dracunculus medinensis
|
|
|
treatment for Dracunculiasis?
|
Worm fragments and pus removed from the lesion.
Administer IV cefazolin & metronidazole (but probably won't be effective) |
|
|
How do you get dracunculiasis?
|
ingesting water in Africa that contains copepods infected by L3 larvae
|
|
|
infective stage of dracunculiasis?
|
3rd-stage larva (ovoviviparous)
|
|
|
Infective stage of wucheria bancrofti?
|
filariform juvenile
|
|
|
vector for wucheria bancrofti?
|
night feeding mosquitos in Africa, Asia and Brazil
|
|
|
clinical manifestations of wucheria bancrofti infection?
|
filarial fever, lymphangitis, lymph stagnation, & lymphedema
Elephantiasis—result of complex immune response due to long-term infection |
|
|
resevoir for Wucheria bancrofti?
|
humans
|
|
|
treatment fo wucheria bancrofti?
|
DOC is diethylcarbamazine.
|
|
|
malayan filariasis is caused by?
|
Brugia malayi
|
|
|
river blindness is also know as?
And caused by? |
onchocerciasis
Onchocerca volvulus |
|
|
vector for onchocerca volvulus?
|
black fly
|
|
|
A Subcutaneous tissue nodule that may be disfiguring but seldom causes pain is associated with?
|
onchocerciasis
|
|
|
Second leading cause of blindness in the world
|
onchocerciasis, a.k.a. river blindness
|
|
|
treatment for onchocerciasis?
|
ivermectin
|
|
|
vector for Loa loa, a.k.a. the eye worm?
|
deer fly in Africa
|
|
|
treatment for Loa loa?
|
surgical removal of worm and adminstration of diethylcarbamazine.
|
|
|
heartworm in dogs is caused by?
Vector? |
Dirofilaria immitis
Mosquito |
|
|
coin lesions on lung x-ray is diagnostic for?
Treatment? |
Dirofilaria immitis
Surgery |
|
|
S. epidermidis is normally a transient bacteremia at best. When is it not?
|
when there is >5 CFU/mL in the blood
Or REPEATED cultures are POSITIVE |
|
|
If S. epidermidis is found in the blood at greater than 5CFU/ml, what does this suggest?
|
IE or Catheter Bacteremia
|
|
|
what is the clinical definition of SIRS?
|
2 or more of the following NOT caused by microbes
- Fever > 100.5 F (38 C) or <97 F (36 C) {normal = 37 C} - Heart rate ≥90 beats per minute {n = 60-80} - Breathing rate ≥ 20 per minute {n = 12} - WBC >12,000/mm3 or <4000/mm3 {n = 4,000-10,000} OR >10% band forms {n = 0-3%} |
|
|
What are the causes of SIRS?
|
NOT microbial infection
- Autoimmune disorders - Pancreatitis - Vasculitis - Burns - Surgery |
|
|
What is the clinical definition of Sepsis?
|
SIRS caused by infection
|
|
|
What is the clinical definiton of Severe Sepsis?
|
Sepsis plus one of the signs of hypoperfusion or organ dysfunction:
- Areas of mottled skin - Capillary refilling requires ≥3 secs - Urine output <0.5 ml/kg for least 1 hour or renal replacement therapy - Lactate >2mmol/L - Abrupt change in mental status - Abnormal EEG findings - Platelet count <100,000 - DIC - ARDS, acute respiratory distress syndrome - Cardiac dysfunction |
|
|
What is the clinical definition of Septic Shock?
|
Sepsis plus 1 or both of the following
a.Systemic mean arterial bp <60 mm Hg (<80 mm Hg, with baseline hypertension) despite adequate fluid resuscitation b.Maintaining bp requires drugs (dopamine, norepinephrine or epinephrine) despite adequate fluid resuscitation |
|
|
what are the three major goals in the treatment of septic shock?
|
1.Resuscitate patient from septic shock - correct hypoxia, hypotension & impaired tissue oxygenation
2.Identify the source of infection & treat w/ antimicrobial therapy; surgery or BOTH 3.Maintain adequate organ system function |
|
|
what is the most significant risk factor for Infective Endocarditis?
|
Residual valvular damage from a previous IE
|
|
|
60yo male presents with abrupt onset of fever, dyspnea, and CNS disturbances. Serology reveals bacteria in the blood. What is the most likely responsible agent?
|
Staph aureus is most likely cause of acute infective endocarditis
|
|
|
60 yo male presents with six week history of low grade fever, weight loss and abdominal distress. Serology reveals bacteria in the blood. What is the most likely responsible agent?
|
viridans streptococci is most likely cause of subacute IE
|
|
|
What is most likely cause of a right sided bacterial IE?
|
S aureus infection of IV drug abuser
|
|
|
82% of IE's are caused by…
|
Staph (42%) and Strep (40%)
|
|
|
Petechiae, Subungual hemorrhages, Osler nodes, Janeway lesions, and Roth spots are all common clinical signs associated with …?
|
microemboli caused by IE
|
|
|
which forms of tularemia infections often lack lymphadenopathy?
|
Typhoidal disease (mentioned as lacking lymphadenopathy or ulcers)
|
|
|
What is the resevoir for the brucella species that is most virulent and causes most cases of brucellosis worldwide ?
|
goats and sheep are the common resevoir for B. melitensis
|
|
|
how is the milde form of brucellosis usually transmitted to humans?
|
drinking unpastuerized milk. B. abortus
|
|
|
why is laboratory diagnosis of tularemia "difficult and dangerous"
|
It's difficult because antibodies cross react with brucella and other species so blood titers are unreliable
It's dangerous because low infectious dose needed for aerosal transmission. So when you culture it, you might spread it to the lab workers. |
|
|
which bartonella species causes Oroya fever and verruga?
Where is it found? |
B. bacilliformis
Restricted to South America |
|
|
Body louse is the vector for which bartonella species?
What is the natural resvoir for this species? |
B. quinana
humans |
|
|
which bartonella species can be transmitted without an arthropod vector?
|
B. henselae can be transmitted through cat scratch or bite
Cat scratch fever = B. henselae |
|
|
what organisms/diseases can the South American sand fly give you?
|
B. bacilliformis - Bartonellosis (acute = Oroya fever. Chronic = verruga)
L. braziliensis - Mucocutaneous Leishmaniasis |
|
|
what organisms/diseases are transmitted by the human body louse?
What regions are they found in? |
Bartonella quintana - bartonellosis (a.k.a. trench fever in WWI)
Rickettsia prowazekii - epidemic (louse-borne) typhus Both are found worldwide in crowded, low socio-economic conditions |
|
|
blood smear showing morulae in neutrophils is diagnositc for which organisms?
|
Ehrlichia and Anaplasma. Region and vector can help distinguish between the two.
|
|
|
vector for Ehrlichia chaffeensis?
|
lone star tick
|
|
|
what is the clinical course of human monocytic ehrlichiosis?
|
After a 1-3 week incubation period, patients develop high fever, headache, and myalgia. Nausea, vomiting, and other non-specific symptoms can occur. A maculopapular rash in about 30% of patients (up to 60% in pediatric cases). Illness is often accompanied by leukopenia, thrombocytopenia, and elevated CRP, ESR, and serum transaminases. Complications include damage to the liver, pulmonary failure, and encephalitis.
|
|
|
9 yo boy from Arkansas presents at clinic with high fever, HA, nausea, and vomiting. Two weeks prior, family had been camping and father pulled three different ticks off his son. Doesn't know the types, but said they didn't all look the same. This morning, parents noticed rash on boys chest and underarms. What is your next logical course of action?
A. Keep the boy hydrated and comfortable in the hospital, and wait for lab identification of causative agent before starting treatment. B. Admit the boy to the hopsital, administering fluids, anti-emetics and IV doxycycline before lab results come back. C. Send him home, telling parentsthat disease is self-limited and they just need to keep him hydrated and comfortable until it goes away on its own. D. Send him howm with prescription of Rifampin, telling parents to keep him hydrated and comfortable and not to to worry when he starts to pee and sweat orange, b/c that's a common side effect of the drug. |
D. doxycycline is contraindicated in children. Use rifampin instead.
|
|
|
tick on a pediatric pt in the SE?
|
Think RMSF. Rickettsia rickettsii
|
|
|
pt from NE with chickenpox-like rash and eschar formation around a bite site?
|
Think rickettsia akari
|
|
|
what causes Boutonneuse fever and where are you if you get it?
|
Caused by rickettsia conorii. Delivered by dog tick in countries around the Mediterranean Sea and parts of Africa.
|
|
|
true or false: Anaplasma phagocytophilum is an intracellular pathogen, taken up by endocytosis and released into the cytosol.
|
False. A. phagocytophilum and E. chaffeensis are both intracellular pathogens taken up by endocytosis, but they remain in vesicles and do not release into the cytosol.
|
|
|
what pathogen might be delivered by a gulf coast tick in the southeastern US?
|
R. parkeri. Causes American Boutonneuse fever
|
|
|
what might rat fleas in urban port cities give you?
|
R. typhi. Causes murine typhus
|
|
|
What causes scrub typhus and where do you get it?
|
Orientia tsutsugamushi
Transmitted by chiggers in East Asia, India, SW Pacific, Australia, Japan, and W. Pacific Islands |
|
|
Recrudescent epidemic typhus is known as…
|
Brill-Zinsser disease. A complication of epidemic (louse-borne) typhus
|
|
|
clinical differences between epidemic and endemic typhus?
|
similar symptoms, but endemic typhus is milder, less likely to produce rash, and only found in warm, humid, populated climates. (warm port cities)
|
|
|
scrub typhus is also found in warm, humid climates. How do you differentiate it clinically from endemic typhus?
|
scrub typhus has necrotic, ulcerated papules
Also, not found in US |
|
|
What's the lab confirmation for rickettsial infections?
|
A four-fold increase in paired sera or an initial titer > 64 (for RMSF) or > 128 (for others) is diagnostic.
|
|
|
Which rickettsia has a vaccine for high-risk populations?
|
r. prowlecki - RMSF
|
|
|
DOC for rickettsial infections?
|
Doxycycline
|
|
|
Small, aerobic, pleomorphic gram-negative bacillus that exists in two forms: SCV and LCV. What is it?
|
Coxiella burnetii. Causes Q-fever.
|
|
|
Farmer presents with 10 day history of high fever, chills, severe headache, myalgia, symptoms of atypical pneumonia and some symptoms of hepatitis. You suspect Q-fever and start patient on doxycycline while waiting for lab work to get back. The lab reports that the patient's blood has more phase II antibodies than phase I. Does this change your treatment plan? If so, what do you do?
|
No change. Phase II antibodies are consistent with Acute Q-Fever infection.
Had there been more Phase I AB than Phase II, you would be looking at Chronic Q-Fever and would need to consult CDC to start patient on combination therapy. |
|
|
What is the infectious form of C. burnettii?
|
Small Cell Variant (SCV)
|
|
|
most common isolate of salmonella?
|
S. Typhimurium
|
|
|
What makes someone more susceptible to salmonella?
What makes someone more resistant to it? |
Patients with achlorhydria are more susceptible, since low stomach acids means it takes a lower inoculum to infect them.
Patients with cystic fibrosis have resistance to salmonella since they have fewer CFTR on their M cells |
|
|
black colonies on an HE plate are indicative of….
|
Sal Typhi
|
|
|
What antigen is specific for Sal Typhi?
|
Vi Antigen
|
|
|
what predisposes sal typhi patient to become chronic carrier?
|
gall stones
|
|
|
What is the best way to recover sal typhi organisms for a lab confirmation of Typhoid Fever diagnosis?
|
Bone Marrow sample is most sensitive - evident 90% of the time - but it is painful to extract.
Stool samples are far easier on the patient and almost as effective - evident in stool in 85-90% of cases So, Check the poo |
|
|
Lab tells me my suspected pneumonia patients's blood shows a "safety pin" on a Wayson stain. What does patient have?
What do I do about it? |
Yersinia pestis - the plague!
Alert CDC and WHO Isolate pt and anyone who has been in contact with pt or lab samples, including myself Start them all on IV/IM Gentamicin Call family and tell them goodbye. 100% mortality rate if not treated in first 24 hrs of contact and the lab took more than 24 hrs to get results. IOW - I'm screwed. |
|
|
Most infectious organism in this unit?
|
Yersinia pestis. A single bacterium can cause infection
|
|
|
cause of death in pneumonic plague?
|
Terminal cyanosis
|
|
|
enteric infection associated with food handlers and travellers to Haiti?
|
Salmonella
|
|
|
what gram negative spirochete causes Lyme disease in North America?
How is it transmitted? |
Borrelia burgdorferi
Spread by Ixodes spp of ticks |
|
|
important things to know about the tick that gives you Lyme disease?
|
Ixodes spp
Adult and nymph are only stages of tick that can infect. Must feed for 48 hrs to transmit Lyme disease Coninfections are common - Ixodes tick is vector for other diseases |
|
|
common coinfections with Lyme disease?
|
Babeseosis - Ixodes vector
Anaplasmosis - Ixodes vector Others - Bartonella, Mycoplasmas, Chronic viral infections (CMV; EBV) - didn't discuss why these are often coinfections |
|
|
A Bull's Eye rash is commonly associated with…
|
Lyme disease
|
|
|
Which clinical symptom are you least likely to find in a patient with Lyme disease?
A. Chills and fever B. Headache C. Diarrhea D. Myalgia E. Lymphadenopathy |
C. Lyme disease has no GI or respiratory symptoms
|
|
|
what is the most effective screening test for Lyme disease?
|
ELISA - Detects anti-Borrelia antibodies
100% Sensitive. No false negatives |
|
|
What is the most effective confirmatory test for Lyme disease?
|
Western blot - Identifies specific proteins of B burgdorferi (not just spirochetes or Borrelia)
100% Specific. No false positives. |
|
|
You were accepted to an allopathic residency in Connecticut (congratulations!). On your first day, you see a patient with a suspected case of Lyme disease. You order labs for confirmation. They come back with a positive ELISA test and a negative Western blot test. Based on these results, which statement below is the MOST accurate statement to tell your attending?
A. Patient may have Lyme disease, but I can't be sure based on these results. B. Based on these results, my patient definitely has Lyme disease. C. I can't confirm Lyme disease, because of the negative Western blot, but, based on the positive ELISA, he is definitely infected with some kind of spirochete. D. Based on these results, my patient definitely does NOT have Lyme disease. E. I don't know anything about Lyme disease, but let me tell you about this patient's CRI... |
A.
|
|
|
what is the most common zoonosis in the world?
|
Leptospirosis
|
