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PHD 6 > PHD 6 > Flashcards

PHD 6 Flashcards

0
Q

Host and vector of dengue fever? Is there a diff inincubation time in the host and the vector?

A

Host–man
Vector– aedes
Incubation period–3-14 days in human host
8-12 days in mosquito vector

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1
Q

What virus family does dengue fever belong to?

A

Flavivirus. It has four serotypes..DEN-1,2,3,4

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2
Q

Do most people with dengue show signs of the infection?

A

No..80-90% of people are asymptomatic or have an undifferentiated fever.

Those who are symptomatic hwever have a breakbone fever.–symptoms are mild to severe.,temps from 102-105, bradycardia, headaches, conjunctivitis and retroorital pain. The pt also experiences severe muscle and joint pain.

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3
Q

Describe the rash that is assoc w/dengue fever

A

It’s present in about 50% of people. It’s a maclar rash that may give rise to petechiae. It starts on the trunk and spreads to the face and the extremities.

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4
Q

What is the transmission cycle of dengue fever?

A

The mosquito feeds on a host that is viremic—EXTRINSIC INCUBATION PREIOD.
Mosquito refeeds and transmits the virus—INTRINSIC INCUBATION PERIOD.

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5
Q

What is dengue hemorrhagic fever?

A

Can’t be distinguished from dengue fever. Characterized by hemorrhage and vascular leak. Pts present w/petechiae, epistaxis, gingival bleeding.

Lab findings–thrombocytopenia and increased Hb (Remember that they’re losing plasma,not blood.

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6
Q

What is the tourniquet test?

A

Inflate bp cuff to a point midway btwn systolic and diastolic for 5 mins.

Positive test:20 or more petechiae per 1 inch squared

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7
Q

What is antibody dependent enhancement?

A

Process in which strains of the denue virus complexed w/ non-neutralizing Abs can enter a greater propotionof celsof the mononuclear lineage and increase virusproduction. The infected monocytes then release vasoactive mediatiors leading to an inc in vascular permeability and hemorrhagic maifestations that characterize DHF.

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8
Q

Detection of dengue fever?

A

Early–PCR

Later NS1 antigen detection

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9
Q

Family, host and vector of yellow fever?

A

Flavivirus, Host is man or primates, Vector is the aedes egypti

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10
Q

Describe the clinical course of yellow fever.

A

BIPHASIC ILLNESS!
Day 1-3 infection
Fevers, chills, malaise, anorexia, nausea, headache, myalgia and backpain

Day 4–remission, symptoms abate

Day 4-10 (intoxication)
fever, nausea, vomiting (black), anxiety, confusion, jaundice, petechiae, elevated liver enzymes and bilirubin, proteinuria, azotemia

Day 7-10 preterminal
Day 10-convalescent

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11
Q

Pathogenesis of yellow fever? Diagnosis of yellow fever/

A

Replicates locally in tissues. Spread via blood to liver, spleen and bone marrow and heart.LIVER is mainorgan affected.

IgG and IgM Abs are used in diagnosing the virus

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12
Q

Is there a vaccine for yellow fever?

A

Yes there is a live attenuated virus, however it can cause a viscerotropic illness in some people.

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13
Q

Which virus causes hantavirus pulmonary syndrome?

A

Sin nombre virus. It is transmitted by infected rodent urine. Remember that a classic thing to look for on blood smear is immunoblasts.

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14
Q

Diagnosis of hantavirus pulm syndrome?

A

Serology–IgG and IgM, immunohistochemistry and RT-PCR.

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15
Q

Host of Lassa fever?

A

Rodents are the host.

Two pearls; Long term sequelae of deafness and responds to ribavarin

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16
Q

Where is the lassa virus found?

A

Found on the West Coast

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17
Q

In which part of the world is Chikungunya endemic?

A

Italy!

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18
Q

How is chikungnya diff fr dengue fever?

A

It usually doesnt have a hemorrhagic component and it presents with joint pain (arthritis) as opposed to muscle pain in dengue.

Similarity; 50% of flks get a rash. Rem however in dengue, you get patches of sparing.

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19
Q

Risk factors for a giardiasis infection?

A

IgA deficiency and achlorhydia

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20
Q

Symptoms of giardiasis?

A

Epigastric pain, nausea, diarrhea

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21
Q

Test of choice in most labs for giardiasis?

A

Stool ELISA

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22
Q

Giardiasis treatment?

A

Treat w/ metronidazole

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23
Q

How would you diagnose cryptosporidiosis?

A

Stool O and P, acid fast staining

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24
Q

What three parasites stain acid fast in the stool?

A

Cryptosporidium, Cyclospora and Cystoisospora

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25
Q

Treatment of cryptosporidisis?

A

Electrolytes (fluid replacement), nitazoxonide. Boil water as a means of prevention.

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26
Q

Apart from acid fast staining what is another mechanism by which cyclosporias can be diagnosed?

A

AUV autofluorescence.

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27
Q

How is entamoeba histolytica transmitted?

A

fecal-oral

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28
Q

Flask shaped ulcers are characterisstic of an infection with this?

A

Entamoeba histolytica

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29
Q

E. histolytica may also affect the liver. What would you expect the lab values to look like?

A

Leukocytosis, no eosinophilia and inc alk phos

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30
Q

Scientific name of the pin worm?

A

Enterobiasis

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31
Q

Descibe the life cycle of the pin worm

A

Direct life cycle–fecal, oral. The eggs are on the perianal folds, they are then ingested by humans, the larvae hatch in intestines of cecum.

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32
Q

How do you diagnose enterobiasis? Treatment?

A

Scotch tape test. Treat w/ albendazole

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33
Q

What is the life cycle of trichuriasis?

A

Direct fecal oral.

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34
Q

How do patients w/ a trichuriasis infection present?

A

Most patients are asymptomatic, if it is a really bad infection, diarrhea may be present, anemia and CHARACTERISTICALLY anal proplapse

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35
Q

How do you diagnose and treat trichuriasis?

A

O and P..look for fotball shaped eggs. Treat with albendazole

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36
Q

Life cycle of Ascaris?

A

Indirect fecal oral. Remember that the eggs first have to mature in the soil. Next it is ingested and the larval stage enters the blood stream—>lungs up the airway and is re swallowed.

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37
Q

Complications of an ascaris infection?

A

Loeffler’ssyndrome (eosinophilia) —> pneumonitis, intestinal obstruction.

38
Q

How do you diagnose Ascaris? Treatment?

A

O and P. Treat w/ Albendazole

39
Q

Hookworm species?

A

Necator americanus and ancylostoma duodenale

40
Q

Life cyle of the hookworm?

A

Eggs in feces—>freeliving L1 to L3–> L3 penetrates the skin—> heart—->lungs—> trachea—-> esophagus—-> STOMACH—–>jejunum

41
Q

Which species of the hookworm causes more blood loss?

A

Ancylstoma duodenale—150 microL as opposed to Necator 40 microL

42
Q

Complications of a hookworm infection?

A

Mostly asymptomatic, ground itch, Loeffler’s syndrome, microcytic anemia since there is actual blood loss.

43
Q

What are the symptoms of a strongylodiasis infection?

A

50% of people have no symptoms..other people present with a ground itch and larva currans. In the lungs, people present with an acute pneumonitis that resembles asthma

In the GI tract—abdominal pain, nausea, anorexia. The immune response is Th2 mediated. IL4—> IgE, IL5—> eosinophils and mast cells are produced

44
Q

What would you expect to see on lab measurements of a strongylodiasis infection? How would you diagnose it?

A

Eosinophilia and anemia. Diagnose w/ O&P, serology, agar culture, Harada-Mori

45
Q

Treatment of a strongylodiasis infection?

A

Ivermectin

46
Q

What is premunition?

A

Persistence of viable organisms at low cncentration within the host. It provides continued immune stimulus to control dz and prevent re-infection

47
Q

IgA deficiency and achlorydia predisposes to this infection?

A

Giardiasis

48
Q

Describe the life cycle of strongyloides, what is auoinfection?

A

3–The larvae develops into free living males and feales. the adults can propagate through several generations of free living worms before infective filariform are again produced. This produces a soil resorvoir that may persist w/o feces deposition

It has 3 different life cycles

#1
Direct life cycle similar to the hook worm. The filariform larvae can penetrate human skin. After they get into the lungs then up the airways they are reswallowed and enter the intestines.
#2
Autoinfection--the larvae passage through the colon to the outside world is delayed and it is transformed to an infective stage without entering the soil. This is the only intestinal nematode that can multiply within the host
49
Q

How does someone get a trichinello infection?

A

Ingestion of muscle conataining the cyst..The larvae then enter the SI, the adults then lay more eggs in the gastric mucosa to perpetuate the infection

50
Q

Discuss the diff in terms of symptoms between the enteral and parenteral phase of a trichinello infection

A

Enteral-asymptomatic usually, it may include nausea, malaise, anorexia, diarrhea and constipation

Parenteral- high fever, facial edema, muscle pain and weakness. There is preferntial involvement of skeletal muscle

51
Q

How is trichinellosis diagnsed?

A

Based on a person’s history, symptoms, presence of eosinophils, serology, biopsy

52
Q

Treatment of trichinellosis? How can this infection be controlled?

A

corticosteroids and albendazole or mebendazole

Control can be achieved by cooking meat well

53
Q

How do people get infected with Toxocara canis?

A

From dogs. They pass the eggs in their feces. If a mammal such as arabbit eats the infected soil, then they become infected. The eggs migrate to the lungs, liver, muscles, heart

54
Q

What is one of the primary manifestations of an infection with toxocara canis?

A

Ocular larva migrans…It may alsso affect other organs –visceral larva migrans leading to eosinophilia, elevated liver enzzymes ;

55
Q

Treatment of Toxocara?

A

Ocular larva migrans–treat w/corticosteroids

Visceral- albendazole, mebendazole +/- corticosteroids

56
Q

How do fols get cutaneous larva migrans?

A

Not from HUMAN hookwrms..but from dog, cattle and sheep hookworm

57
Q

How does cutaneus larva migrans present?

A

Creepin eruption..since it doesn’t know exactl where to go in humans. People present w/ papules, edema, itching

58
Q

Diagnosis and treatment of CLM?

A

Skin biopsy and treat w/ albendazole

59
Q

Transmission cycle of dracunculiasis?

A

Larvae are consumed by cocepds..humans drink contaminated water..after the copepods die, the larvae are released and reproduce. The pregnant female migrates to the surface f the skin..causes a blister. When it erupts, more larvae are released to continue the cycle.

60
Q

How does dracunculiasis present?

A

No symptoms for about a year then persons present w/ non specific symptoms–nausea, vomiting, diarrhea, rash, dizziness, fever

61
Q

How is the life cylce of dracunculiasis perpetuated?

A

The blister that forms is burning in quality..therefre people immerse their feet w/ water the female then emerges

62
Q

What are some complications of dracunculiasis?

A

Local/systemic infection, tetanus, pain and disability`

63
Q

Transmission cycle of lymphatic filiriasis?

A

The microfilaria form mature in the mosquito’s gut. It is transmitted when the mosquito takes a blood meal from a human. Rem these mosquitoes usually feed @ night

64
Q

Difference in disease manifestation between the adult worms and filaria?

A

Diseases due to adult worms is usually a consequence f worm demise followed by fibrosis.

Filaria may cause TPE (Tropical pulmonary eosinophilia syndrome)–kinda like Loeffers but more severe. It presents with a cough, fever, increased eosinophils and increased IgE

65
Q

Diagnosis of filiriasis? Treatment?

A

Blood smear btwn 10pm and 2am

Treat with DEC, ivermectin and doxy

66
Q

What causes African River blindness?

A

Onchocerciasis–The black fly takes a bloodmeal, enters subcutaneous tissue and makes a subcutaneous nodule. Adults produce microfilaria and the black fly then takes a blood meal to perpetuate the infection

67
Q

How is an infection with onchocerciasis manifested?

A

Chronic papular dermatitis, subcutaneous nodules, leopard skin

68
Q

How does the blindness come about in persons with African River blindness?

A

The inflammation is caused by the wolbachia virus carried by the microfilaria.

69
Q

How do you diagnose an infection with onchocerciasis?

A

Skin snips..treat w/ ivermectin (CONTRAINDICATED IN PTS WITH LOIASIS)
Doxy

70
Q

Which drug is contraindicated in patients with onchocerciasis?

A

Mazzoti reaction–intense inflammation and skin sloughing

71
Q

How is Loa La transmitted?

A

It is transmitted by the mango fly.The adults enter subQ tissue and the microfilaria enter the body fluids. When another fly takes a blood meal the cycle continues.

72
Q

How does a Loa Loa infection manifest?

A

Calabar swelling–localized angioedema associated w/ puritis. The adult worms live in connective tissue between the skin and fascia

73
Q

Of DEC, Ivermectin, Albendazole and doxy, which one kills microfilariae?

A

all but doxy

74
Q

Of DEC, Ivermectin, Albendazole and doxy, which ones kill he adults in filiriasis?

A

Doxy and DEC in Loa, Loa

75
Q

Drug of choice for treating lymphatic filiriasis?

A

DEC

76
Q

DEC is contraindicated in the treatment of?

A

Onchocerciasis

77
Q

Drug of choice for Loiasis if low MF counts?

A

DEC

Albendazole

78
Q

Which insect transmits Leishmaniasis?

A

Sand fly. The promastigotes in the gut of the sand fly enter the lymph or blood of human. Ther mature to amastigotes which replicate by binary fission. The amastigotes enter the macrophages

79
Q

What are the three forms of a Leishmania infection?

A

Cutaneous- Mucocutaneous and Kala azar (Visceral)

80
Q

Describe the presentation of the cutaneous form of Leishmania/

A

Most common,usually a painless nodule. They may follow the lymph nodes. The scars spontaneously heal.

81
Q

Where is the mucocutaneous infection w/ Leishmania ltd to? How does t present?

A

Ltd to C and S America. Initially it looks like cutaneous leishmani then ulcers develp[ in nose, muth and throat. It is very disfiguring

82
Q

Clinical course of a visceral Leishmani infection?

A

Symptoms are usually delayed. They present with a fever, weight lloss, spleno/hepatomegaly, adeopathy and dark skin. IT IS FATAL IF UNTREATED.

83
Q

Treatment of Cutaneous Leishmania? How about visceral?

A

Pentavalent antimonial compunds IM

Amphotericin B

84
Q

Prevention of Leishmania?

A

Suppress the resorvoir (dogs rates, etc)
Suppress the vector
Prevent sandfly bites–long sleeves, repellant, permethrin treated uniforms and bed nets

85
Q

Transmitted by the reduvid bug?

A

Chagas dz

86
Q

Buzz word: Romanas sign?

A

Chagas dz–onset is immediate, it lasts weeks to months. Fever, localized swelling near the bite (Romano’s sign)

87
Q

If Chagas dz progresses to the chronic stage, what organs are usually affected?

A

Heart–get an apical aneurism

Colon–get a mega colon

88
Q

What are the indications for treatment of Chagas dz?

A

Acute/Reactivated dz

<18

89
Q

What are the two speces of Trypanosomes?

A

T brucei gambiense–West African sleeping sickness

T brucei rhodesiense– East African sleeping sickness

90
Q

Vector for Trypanosome infection?

A

Tsetse fly.

91
Q

Diff btween T. brucei and T. rhodisiense.

A

T. brucei (main resorvoir is man). Clinically the infected person has fevers, headaches, muscle, joint pain. They also have Winterbottom’s sign (occipital sign). They exp personality changes sleep disturbances, confusion, paralysis may occur. Kills in abt 3 years

T. rhodisiense–Main resorvoir is cattle. Infected persons may develop a chancre at the bite site. Paint wll get a fever, muscle , joint aches.
After a few weeks of infection, mental detioration may occur, death usually occurs in a few months
T

92
Q

An infection w/ Babesiosis means that the person probably lived where?

A

In the North East.

93
Q

Maltese cross and multiply infected RBC are indicative of an infection w/?

A

Babesiosis–rem it is protective against ticks.

PHD 6 (1 decks)

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