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Term 5: Infectious Disease > 6/22: Protozoans III: Toxoplasmosis and Malaria > Flashcards

6/22: Protozoans III: Toxoplasmosis and Malaria Flashcards

1
Q

Humans are ___ hosts of Toxoplasma gondii?

A

Humans are intermediate hosts of Toxoplasma gondii

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2
Q

Cats are the ___ hosts of Toxoplasma gondii?

A

Cats are the definitive hosts of Toxoplasma gondii; the actual life stages occurs in those hosts

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3
Q

Life cycle of T. gondii in cats?

A
  • Infected by carnivorism of tissue cysts (containing dormant bradyzoite) ingested by the cat
  • Viable organisms are released and trophozoites/tachyzoites invade epithelial cells of small intestine
  • Undergo sexual cycle and produce oocysts which are excreted

So the three forms are:

  • Trophozoite/tachyzoite (invade tissues)
  • Dormant bradyozoite (in tissue cysts)
  • Oocyte (excreted by cats)
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4
Q

How can humans be infected with T. gondii?

A
  • Ingestion of undercooked infected meat containing Toxoplasma cysts
  • Ingestion of oocyst from fecally contaminated hands or food
  • Organ transplantation or blood transfusion
  • Transplacental
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5
Q

What is this? Which end is front?

A

Tachyzoites (of T. gondii)

  • Tapered anterior end
  • Blunt posterior end and large nucleus

Found in various sites throughout body of host

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6
Q

What is this? Found where?

A

Tissue cysts of T. gondii

  • Most commonly in skeletal muscle, myocardium, and brain
  • May remain throughout life of the host
  • Typ spherical in the brain but more elongated in cardiac/skeletal muscle
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7
Q

Where in the world is T. gondii normally found?

A

High prevalence in France (related to eating raw/undercooked meat)

  • up to 90% by age 30-40

US:

  • 5-45% of population is seropositive

Congenital infection

  • 0.1% of pregnancies
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8
Q

Acute infection of T. gondii presents how? Sx last how long?

A
  • Often asymptomatic in immunocompetent persons
  • Cervical lymphadenopathy and/or mononucleosis-like illness (10-20%)
  • Clinical course typ benign and self-limited with symptoms resolving within a few months to a yr
  • Ocular Toxoplasma: retinochoroiditis (from congenital infxn or infxn after birth)
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9
Q

Characteristics (of spread) of congenital Toxo?

A
  • Results from acute primary infection acquired by mother during pregnancy
  • Chance of infection is greater with advancing gestational age at the time of maternal linfxn (but severity worse if earlier infection?)
  • Treatment of mom may reduce incidence of congenital infection and reduce sequelae in infant
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10
Q

Symptoms of congenital Toxo?

A

Fetal infection may lead to:

  • Intracranial lesions
  • Disseminated infxn in early infancy
  • Serious neurological impariment
  • Retinochoroiditis

Ocular Toxoplasma (from congenital infxn or infxn after birth)

  • Causes retinochoroiditis
  • Pt often asymptomatic until 20s/30s when lesions develop in the eye
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11
Q

Reactivation infection of Toxoplasmosis is possible in what hosts?

A
  • AIDS
  • Transplant patients

Usually caused by reactivation of chronic infection

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12
Q

Primary symptoms of reactivation infection of Toxo?

A
  • Encephalitis or CNS mass lesion (picture)
  • Rarely chorioretinitis or pneumonitis
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13
Q

What is this?

A

Ocular Toxoplasma (from congenital infxn or infxn after birth)

  • Causes retinochoroiditis
  • Pt often asymptomatic until 20s/30s when lesions develop in the eye
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14
Q

How do you diagnose Toxoplasmosis?

A

Serologic testing is the routine method of diagnosis

Also:

  • Observation of parasites in pt specimens (e.g. BAL material or LN biopsy)
  • Isolation of parasites from blood or other body fluids, by intraperitoneal inoculation into mice or tissue culture
  • Detection of parasitic genetic material by PCR, esp in detecting congenital infxns through amniocentesis
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15
Q

Who needs to be treated for Toxoplasmosis?

A
  • Not need for healthy non-pregnant person (Sx will usually go away within few weeks)
  • Do need to treat compromised pts, pregnant women, and newborns
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16
Q

Treatment of Toxo: AIDS?

A

AIDS: 4-6 wks of primethamine and sulfadiazine

Alternatively: cinda/pyrimethamine

  • Followed by suppressive therapy
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17
Q

Treatment of Toxo: Congenital?

A

1 yr of pyrimethamine and sulfonamide

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18
Q

Treatment of Toxo: Women in 1st TM? After 1st TM?

A

1st TM: Spiramycin

> 1st TM without transmission to fetus: Spiramycin

> 1st TM with transmission in utero: Pyrimethamine and Sulfadiazine

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19
Q

Characteristics of Spiramycin for treatment of Toxoplasmosis?

  • Class
  • Delivery
  • Method
  • Adverse side effects
A
  • Macrolide
  • Oral
  • Inhibits growth of susceptible organisms (mech unknown)
  • Side effects: GI, prolonged QT
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20
Q

Characteristics of Pyrimethamine for treatment of Toxoplasmosis?

A
  • Dihydrofolate reductase inhibitor (folic acid antagonist)
  • Long-acting
  • Most effective agent for Toxoplasmosis

Toxicity:

  • Dose related suppression of bone marrow; decreased by giving folinic acid (Ca leucovorin)
  • GI distress, rash, headache, bad taste in mouth
  • Potential teratogen; only use after 1st TM!!
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21
Q

Characteristics of Sulfadiazine for treatment of Toxoplasmosis?

A
  • Sulfonamide
  • Intermediate-acting
  • Acts synergistically with pyrimethamine

Toxicity:

  • Skin rashes (sometimes life-threatening)
  • Crystal induced nephrotoxicity
  • Hallucinations, new onset of psychiatric symptoms
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22
Q

What is the treatment of choice for Toxo?

A

Combo of Pyrimethamine and Sulfadiazine

  • Response rates 68-95%
  • Limited by toxicity (but used ubiquitously in AIDS pts) ((Single most efficient agent is Pyrimethamine)
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23
Q

How to treat someone with Toxo who’s allergic to sulfa drugs?

A

Pyrimethamine and Clindamycin

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24
Q

Characteristics of Clindamycin for treating Toxoplasmosis?

A
  • Acts by targeting transplantation in the apicoplast of T. gondii
  • Acts synergistically with pyrimethamine

Toxicity:

  • Rashes
  • Nausea/vomiting (if oral; not with IV)
  • Diarrhea; may be associated with C. difficile infection

(Also limited to toxicity)

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25
Q

Alternative Toxo Treatments? When to use? Characteristics?

A

Trimethoprim/Sulfamethoxazole (Bactrim)

  • Not 1st line, but used for prophylaxis for toxo and pneumocystis
  • Used in treatment of Isospora and Cyclospora infxns
  • Toxicity: bone marrow suppression, rash, elevated liver enzymes, interstitial nephritis, nausea/vomiting

Pyrimethamine & Folinic Acid and one of:

  • Atovoquone - Clarithromycin - Azithromycin - Dapsone
  • These have been used in clinical studies with few pts and have response rates lower than the standard regimens
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26
Q

What is the #1 cause of parasitic death?

A

Malaria

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27
Q

Incidence of Malaria?

A
  • 41% of world’s population live in area where malaria is transmitted
  • 350-500 million cases/yr with over 1 million deaths (mostly young children in sub-Saharan Africa)
28
Q

Geography of Malaria?

A
  • 90% of deaths occur in Sub-Saharan Africa
  • Local weather conditions allow transmission to occur year-round
  • Scarce resources and socio-economic instability hinder efficient malaria control activities
29
Q

What is the vector for Malaria?

A

Mosquito (Anopheles gambiae)

  • Very efficient
30
Q

What is the predominant parasite species causing Malaria?

A

Plasmodium falciparum

  • Causes the most severe form of malaria
31
Q

Malaria in the US?

A
  • Formerly common
  • Has been eradicated for > 50 yrs, but few deaths still reported (all but 5 were imported)
  • Constant risk that malaria could be reintroduced in the US (Anophelenes are prevalent) Potential malaria vectors in US (picture)
32
Q

The __ species of Plasmodium that infect humans in nature are:

A

Four:

  • Plasmodium falciparum
  • Plasmodium vivax
  • Plasmodium ovale
  • Plasmodium malariae
33
Q

Characteristics of human malaria from P. falciparum?

A
  • Only species that can cause severe, potentially fatal, malaria
  • Multiplies rapidly in blood
  • Parasite-infected RBCs can clog small BVs; this causes cerebral malaria in the brain (quickly fatal)
34
Q

Characteristics of human malaria from P. vivax?

A
  • Found mostly in Asia, Latin America, and some parts of Africa
  • Only exceptionally causes death (most often due to rupture of enlarged spleen)
  • But symptoms are often incapacitating
35
Q

Characteristics of human malaria from P. ovale?

A
  • Less frequently encountered than falciparum and vivax
  • Found mostly in W Africa and islands of W Pacific
  • Biologically and morphologically similar to P. vivax
36
Q

Characteristics of human malaria from P. malariae?

A
  • Less frequently encountered than falciparum and vivax
  • Found worldwide
  • Causes a long-lasting, chronic infection that can last a lifetime
  • Can cause nephrotic syndrome
37
Q

Life cycle of plasmodium causing malaria?

A
  • Female Anopheles mosquito inoculates sporozoites into human host
  • Sporozoites infect liver cells and mature into schizonts, which rupture and release merozoites
  • In P. vivax and P. ovale: a dormant stage (hypnozoite) persists in liver and cause relapse by invading the bloodstream wks-yrs laters
  • After initial replication in the liver (exo-erythrocytic schizogony), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony)
  • Merozoites infect RBCs
  • Ring stage trophozoites mature into chizonts, which rupture and release merozoites
  • Some parasites differentiate into sexual erythrocytic stages (gametocytes), which transmit the infection to mosquitoes
  • Blood stage parasites are responsible for the clinical manifestations of the disease
  • Sexual reproduction occurs within the mosquito
38
Q

Common presenting symptoms of malaria? Physical findings?

A
  • Fever
  • Chills
  • Sweats
  • Headaches
  • Nausea/vomiting
  • Body aches
  • General malaise
  • Always consider malaria in patients presenting with fever in an endemic area or who have traveled or immigrated from an endemic area

Physical findings:

  • Elevated temperature
  • Enlarged spleen
  • Mild jaundice and enlargement of liver (P. falciparum)

Classically (but infrequently seen) attacks of fever and associated Sx occur every 2nd day with the “tertian” parasites (falciparum, vivax, ovale) and every 3rd day with “quartan” (malariae)

39
Q

Manifestations of severe malaria? Caused by what?

A

Severe malaria caused by P. falciparum only

  • Severe hemolytic anemia
  • Cerebral malaria, manifested by: altered mental status, seizures, coma
  • May also have acute kidney failure (from sludging/anoxia and from hemoglonbinuria)
  • Pulmonary edema or ARDS can occur after parasite counts have decreased in response to treatment
  • Hypoglycemia- esp in children and pregnant women
  • Cardiovascular collapse and shock

Severe malaria is a MEDICAL EMERGENCY; must be treated aggressively (may die within 12 hours)

40
Q

Who normally gets severe malaria?

A
  • People with no immunity to malaria (people from areas with low/no malaria transmission)
  • People with decreased immunity (young children and pregnant women in areas with high transmission)
41
Q

How is malaria diagnosed?

A

Demonstration of malaria parasites on blood smear under microscope

  • Thick or thin blood smear
  • Stained with Romanowsky stain
  • Examined at 100x under oil

Rapid diagnostic tests (RDTs) or immunochromatographic tests are a useful alternative to microscopy if not available (in progress)

  • Binax NOW is the only brand approved in the US
42
Q

Light microscopy characteristics of malarial species?

A

P. vivax/ovale/malariae:

  • Usually only 1 ring form per RBC, under 1% of RBCs infected
  • Trophozoite appears ameboid with irregular shape (enlarging forms)
  • Large coalescent pigment. 12-18 parasite nuclei within each RBC (dividing forms)
  • Round gametocytes

P. falciparum:

  • May have multiple ring-form organisms per RBC, > 1% RBCs infected
  • Enlarging forms and dividing forms are rare in blood (already clotted up somewhere in peripheral blood/organs)
  • Banana-shaped gametocytes
43
Q

What is this?

A

Plasmodium falciparum

  • Can see multiple ring-form organisms per RBC
  • Bottom right = gametocyte
44
Q

What is this?

A

Plasmodium vivax/ovale/malariae

  • Top left = amoeboid
  • Top center = multiple merozoites
  • Top right = larger cell with Sch– dots (vivax?)
  • Bottom right = band-type trophozoite (malariae)
45
Q

Treatment of malaria depends on what?

A
  • Species of plasmodium
  • Area where infection was acquired and its drug-resistance status
  • Clinical status of the patient
  • Pregnancy
  • Drug allergies or other meds taken by pt
46
Q

Drugs used in treatment of malaria work how? They include?

A

Most are active against parasite forms in the blood:

  • Chloroquine
  • Sulfadoxine-pyrimethamine
  • Mefloquine
  • Atovaquone-proguanil
  • Quinine
  • Doxycycline
  • Artemisin derivatives
47
Q

Recommended treatment for uncomplicated malaria (non-resistant)?

A

For P. falciparum acquired in areas without chloroquine-resistant strains

  • Central America west of Panama Canal, Haiti, Dominican Repulbic, and most of Middle East Oral chloroquine
  • 600 mg base (1000 mg salt) followed by 300 mg base (500 mg salt) at 6, 24, and 48 hours after initial dose
48
Q

Characteristics of Chloroquine for treatment of malaria?

  • Form
  • Kinetics
  • Target
  • Resistance?
A
  • Oral
  • Long half life (allows weekly dosing for prophylaxis)
  • Active against the asexual erythrocytic stage of sensitive Plasmodium species
  • Used as mainstay of treatment and chemoprophylaxis
  • Limited use since chloroquine-resistant P. falciparum
49
Q

Mechanism of Chloroquine for treatment of malaria?

A
  • Parasite causes degradation of hemoglobin, so releases Ferriprotoporphyrin IX
  • Ferriprotoporphyrin IX (soluble form) inhibits parasitic enzymes
  • Plasmodium species have a heme polymerase that makes Ferriprotoporphyrin IX insoluble
  • Chloroquine inhibits the heme polymerase
50
Q

Toxicity of Chloroquine for treatment of malaria?

A
  • Nonspecific GI and CNS Sx
  • Pruritis
  • Retinal damage with long term,high dose therapy in persons with collagen vascular disease
51
Q

Recommended treatment for malaria (resistant)?

A

For P. falciparum infections acquired with chloroquine-resistant strains, there are 3 options:

  1. Quinine sulfate + doxycycline or tetracycline or clindamycin
  2. Atovaquone proguanil (Malarone)
  3. Mefloquine- now 3rd line (neuropsychiatric side effects)
52
Q

Characteristics of Quinine for treatment of malaria?

A
  • Oral (IV not available in US)
  • Rapidly absorbed
  • Short half-life; dosed several times a day
  • Oldest antimalarial drug (S American Indian wi/ cinchona bark)
  • Rapidly active against asexual erythrocytic stage of Plasmodium
  • Resistant strains found in Thailand

Toxicity:

  • Cinchonism (with higher doses): nausea/vomiting, tinnitus, disturbed vision, GI complaints
  • Hypoglycemia with high P. falciparum parasitemia due to insulin release
  • Stimulates uterine contraction; may induce abortion
  • Myocardial depression: hypotension, respiratory depression, and death in overdoses
53
Q

Characteristics of Doxycycline for treatment of malaria?

A
  • Broad spectrum tetracycline Abx
  • Active against all Plasmodium species
  • Oral
  • Short half-life; dosed daily
  • Used for prophylaxis
  • In treatment used with combination b/c effects are slow

Toxicity:

  • Diarrhea (C. difficile in older pts)
  • Concentrated in bones and teeth -> dental staining, hypoplasia of dental enamel, impaired bone growth in fetus/young child, contraindicated in pregnancy and children under 8 (teratogenic)
  • May -> sunburn predisposition
54
Q

Characteristics of Malarone for treatment of malaria?

A
  • Atovaquone/Proguanil
  • Active against chloroquine-resistant P. falciparum and other species
  • Active against liver stages so prophylaxis can be stopped sooner than other agents
  • Oral combination pill
  • Prophylaxis: one pill a day (2-3 days prior to trip, while on trip, and 7 days after)
  • Also used to treat uncomplicated malaria
  • Minimal toxicity: rash, fever
55
Q

Characteristics of Mefloquine for treatment of malaria?

A
  • Active against asexual erythrocyctic state of Plasmodium species
  • Mefloquine-resistant P. falciparum along Thai borders
  • Orally absorbed
  • Long half-life – weekly dosing for prophylaxis

Doses (Adult):

  • Prophylaxis: 1 pill (250mg) a week
  • Acute malaria (non-severe): 5 pills in two doses

Toxicity:

  • Neuropsychiatric effects
  • Syncope
  • Depression
  • Dizziness
  • Rare: psychosis/seizures
56
Q

Treatment of choice for malaria?

A

Chloroquine for:

  • P. malariae
  • P. vivax: unless from Papua New Guinea or Indonesia (widespread resistance; may also be emerging in Myanmar, India, and S America)*
  • P. ovale

*Initially treat with chloroquine and then change to Quinine + Doxycycline/Tetracycline/Mefloquine if poor rsponse

Primaquine for:

  • P. vivax and P. ovale since they may relapse due to hypnozoites
  • Treat for 14 days
57
Q

Characteristics of Primaquine in treatment of malaria?

A
  • Oral
  • Short half-life, dosed daily
  • Active against liver stages including hypnozoites of P. vivax and P. ovale, and against gametocytes
  • Administered after chloroquine treatment

Toxicity:

  • Severe hemolytic anemia in pts with G-6-PD deficiency; contraindicated in pregnancy (b/c don’t know with fetus?)**
  • GI symptoms
  • High doses, but rare: Methemoglobinemia and blood dyscrasias

**Pregnant patients with P. vivax or P. ovale should be maintained on weekly chloroquine prophylaxis for the duration of pregnancy and then with primaquine after delivery (if not G6PD deficient)

58
Q

How should severe malaria be treated?

A

Immediately! Medical emergency

  • Antimalarial therapy for pts with manifestations of severe disease
  • Treatment for falciparum malaria in case of mixed infection/misdiagnosis if their is clinical evidence of severe malaria but blood smear is reported as vivax, ovale, or malariae
59
Q

What is the drug of choice for pts requiring parental therapy for malaria?

A

Artesunate

  • More effective than quinine and safer than quinidine (alternatives if artesunate not available)
  • Usually given over 3 days at 0, 12, 24, and 48 hours
  • Should be accompanied as soon as possible by an oral drug (Malarone, Doxycycline, Clindamycin or Mefloquine)
60
Q

Characteristics of Artemisinins (Artesunate) in treatment of malaria?

A
  • Oral, IV, and rectal forms
  • From Artemisia annua a Chinese weed (wormwood plant) - Kills erythrocytic forms
  • Used globally for treatment; available in US – via CDC
  • Should be given with combination (eg., doxycycline or mefloquine) to avoid resistance and relapses

Toxicity is infrequent and mild:

  • Anemia, leukopenia
  • Elevated liver enzymes
  • Abdominal pain/diarrhea
  • Drug fever
  • Contraindicated during 1st TM of pregnancy; use with caution in 2nd and 3rd TM
61
Q

Characteristics of Quinidine for treatment of malaria?

A
  • Isomer of quinine
  • Short half-life, dosed several times a day
  • May use for severe malaria in the US when oral therapy not possible
  • IV tx in US for severe malaria, until Artesunate obtained; can be switched to oral medication (quinine) after at least 24 hrs of IV tx and when parasitemia is
62
Q

Outcomes of malaria in pregnancy?

A
  • Miscarriage
  • Premature delivery
  • Low birth weight
  • Congenital infection
  • Perinatal death
  • Associated with high risks of both maternal and perinatal morbidity and mortality
  • Pregnant women have a reduced immune response and thus clear malaria infections less effectively
  • Pregnant women are 3x more likely to develop severe disease than non-pregnant women (more hypoglycemia, more anemia, more respiratory complications- pulmonary edema, ARDS)
63
Q

How to deal with malaria in pregnancy?

A

Intermittent preventative therapy (IPT) with:

  • Sulfadoxine-pyrimethamine for pts who reside in areas of high/medium malaria transmission
  • Administered 2x after onset of fetal mvts (about 16 wks)
  • This has replaced weekly chloroquine prophylaxis as the preferred method
  • Monthly IPT is recommended for HIV+ pregnant women

For uncomplicated malaria from malariae/vivax/ovale/chloroquine-sensitive falciparum

  • Treat with chloroquine (or hydroxychloroquine)

For uncomplicated malaria caused by chloroquine-resistant falciparum:

  • Treat with quinine sulfate and clindamycin

*Quinine treatment should continue 7 days for infxns from Southeast Asia and 3 days if from Africa/S AMerica

*Clindamycin should continue for 7 days regardless of where infection was required

For chloroquine-resistant P. vivax:

  • Treat with Mefloquine or quinine for 7 days

*Mefloquine now considered category B and may be used for treatment or prophylaxis in pregnant women

*For uncomplicated malaria, Artemenisin derivatives are safe in 2nd or 3rd TM but more data needed for non-urgent 1st TM use

*Doxycycline and tetracycline are generally not indicated for use in pregnant women; may rarely be used in combo with quinine if other options not available or tolerated and benefit > risk

*Atovaquone/proguanial is category C and not indicated in pregnancy; may be used in uncomplicated chloroquine-resistant P. falciparum if other options not available or tolerable and benefit > risk (no data in treatment of chloroquine resistant P. vivax infections)

*Again, for P. vivax or P. ovale infections, primaquine phosphate for radical treatment of hypnozoites- should not be given during pregnancy.

* Pregnant patients with P. vivax or P. ovale infections should be maintained on chloroquine prophylaxis for the duration of their pregnancy

* After delivery, pregnant patients with P. vivax or P. ovale infections who do not have G6PD deficiency should be treated with primaquine.

SEVERE MALARIA:

  • For chloroquine-resistant malaria, parenteral therapy with either artesunate or quinidine, plus clindamycin
  • Artemisinin derivatives are safe in 2nd/3rd trimester, and are now recommended even in the first trimester for severe malaria
  • Quinine and quinidine can be used in pregnant women with P. falciparum infections at recommended therapeutic doses, and do not lead to adverse pregnancy outcome compared to the malaria infection itself
  • Clindamycin, azithromycin and proguanil are also safe; folate supplementation is recommended with proguanil.
64
Q

Characteristics of Fansidar in treatment of malaria?

A

- Pryrimethamine and Sulfadoxine

  • Sequential blockade of two steps in the folic acid metabolic pathway
  • Active against asexual stage
  • Initially active against chloroquine-resistant P. falciparum, resistance spreading
  • Oral, well absorbed
  • Long half-life; single dose treatment

Toxicity: mainly due to sulfonamide:

  • GI sx
  • Allergic reactions
  • Rash
  • Hepatitis
  • Bone marrow suppression
65
Q

Prevention of malaria in endemic areas?

A
  • Vector control
  • Personal protection measures like insecticide-treated bed nets
  • Antimalarial drugs for vulnerable groups (pregnant women get IPT Fansidar)
66
Q

Prevention of malaria in travelers?

A
  • Refer to CDC/WHO guidelines looking specifically at drug resistance patterns of the region and recommended prophylactic meds
  • No drug guarantees protection against malaria. Travelers should seek medical attention if they develop a fever before/after return
  • Insect repellents (DEET), insecticide-pregnated bed nets (permethrin) and proper clothing
  • Malaria in pregnancy is particularly serious for both mother and fetus; prophylaxis indicated if exposure cannot be avoided

Term 5: Infectious Disease (18 decks)

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