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Microbiology Exam V > Parasitic Infections of the Circulatory, Reticuloendothelial, and Lymphatic Systems > Flashcards

Parasitic Infections of the Circulatory, Reticuloendothelial, and Lymphatic Systems Flashcards

1
Q

Protozoa (Disease, Vector, Intracellular Stage)

A

1) African Trypanosomiasis (T. brucei) –> Tsetse flies –> No intracellular stage
2) Chagas’ Disease (T. cruzi) –> Reduvid Bugs –> Skeletal and Cardiac Muscle Cells
3) Leishmaniasis (Leishmania spp.) –> Sandflies –> Macrophages
4) Malaria (Plasmodium spp.) –> Mosquitoes –> RBCs and Hepatocytes
5) Babesiosis (Babesia spp.) –> Ticks –> RBCs

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2
Q

Trypanosoma brucei - Sleeping Sickness - African Trypanosomiasis

A

Only in AFRICA
Tsetse fly
Some species have animal reservoir
“Nagana” in cattle

Flagellated protist that develops in the gut of the Tsetse fly

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3
Q

Trypanosoma brucei - Sleeping Sickness - African Trypanosomiasis (Disease Progression)

A

Painless hard nodule where fly bit –> Parasite multiples in bloodstream, lymphatics –> CNS –> Lymphadenopathy on back of neck –> WASTING APPEARANCE –> Meningioencephalitis

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4
Q

Trypanosoma brucei - Sleeping Sickness - African Trypanosomiasis (Forms)

A 
West African (T. brucei gamiense)
-Human to human spread
East African (T. brucei rhodesiense)
-Human to human and animal to human

Early Stage: organisms in blood/peripheral lymph nodes
-Fever, myalgia, chills, lymph node swelling (West)

Late Stage: Invasion of CNS
-Headaches, seizures, tremors, encephalitis, periods of sleeplessness and lethargy, coma and death

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5
Q

Trypanosoma brucei - Sleeping Sickness - African Trypanosomiasis (Diagnosis and Control)

A

East African form:
-Shorter incubation (2-3 weeks) and faster CNS involvement (3-4 weeks)
West African form:
-Longer incubation (weeks to months) and longer til CNS involvement (weeks to years)

Diagnosis: Blood smears (detect parasites), lymph node aspirates, or CSF

Control disease by controlling flies

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6
Q

Trypanosoma brucei - Sleeping Sickness - African Trypanosomiasis (Immune System Avoidance)

A
  • ANTIGENIC VARIATION*
  • Trypanosomes rapidly switch their surface antigenicity (glycoproteins) preventing absolute clearance of all organisms

Leads to a PATTERN OF SPIKES OF PARASITES

VSG (150 different genes that encode this variant surface glycoprotein)

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7
Q

Trypanosoma brucei - Sleeping Sickness - African Trypanosomiasis (Treatment)

A

Melarsoprol (TOXIC) 80% effective at best
-5% develop encephalopathy

Difluormethylornithine (DFMO)

  • Doctors Without Borders
  • The French
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8
Q

Trypanosoma cruzi - Chagas’ Disease - American Trypanosomiasis (Life Cycle)

A

Similar to Trypanosoma brucei (Flagellated protozoan, insect bite, etc.)

***Intracellular form called Amastigotes (cause cardiac problems, GI problems - Megacolon and Megaesophagus)

Parasites come out of rear of bug (Reduvid Bug) as it is taking a blood meal, rub feces/parasites into bite

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9
Q

Trypanosoma cruzi - Chagas’ Disease - American Trypanosomiasis (Epidemiology)

A

SOUTH AND CENTRAL AMERICA

USA rare –> due to immigration

  • US Blood Supply*
  • 1 / 30,000 donated units test positive for anti-T. cruzi antibodies
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10
Q

Trypanosoma cruzi - Chagas’ Disease - American Trypanosomiasis (Transmission and Symptomology)

A

Transmission:

  • Bite/Defecation of infected Reduvid Bug
  • Blood transfusion

Symptomology:

  • First sign of infection is development of CHAGOMA (hard red nodule)
  • Romana’s Sign*
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11
Q

Trypanosoma cruzi - Chagas’ Disease - American Trypanosomiasis (Acute vs. Indeterminate vs. Chronic Phase)

A

Acute:
-Fever, malaise, myalgia, and HEPATOSPLENOMEGALY

Indeterminate (Asympatomic):

  • Few parasites in blood. HIGH LEVELS OF ANTIBODY
  • Most individuals remain in this phase for life*

Chronic Disease (10-30% of individuals):

  • Infection of CARDIAC MUSCLE and MYENTERIC PLEXUS
  • Develops years to decades after infection
  • Cardiac and GI involvement (CHF, Megacolon, Megaesophagus)
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12
Q

Trypanosoma cruzi - Chagas’ Disease - American Trypanosomiasis (Diagnosis)

A

Acute phase: detection of parasites in peripheral blood

Chronic disease: serology

Travel history consistent with exposure

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13
Q

Leishmania spp. - Leishmaniasis (Characteristics)

A

Sand Fly (female) = Vector

Intracellular pathogens of MACROPHAGES and MONOCYTES

2 million new cases annually, although RARE in the US

Increasingly recognized as an opportunistic pathogen in HIV+ individuals
-Primarily in the MEDITERRANEAN

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14
Q

Leishmania spp. - Leishmaniasis (Reservoirs and Clinical Presentations)

A

Reservoirs: Canines and Rodents

Clinical Presentation:

1) Cutaneous (L. major, L. tropica, L. mexicana)
2) Mucocutaneous (L. braziliensis)
3) Visceral (L. donovani, L. infantum, L. chagasi)

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15
Q

Leishmania spp. - Leishmaniasis (Visceral)

A
  • Involves the dissemination of parasites throughout the reticuloendothelial system. Parasites can be found in MACROPHAGES of the LIVER, SPLEEN, BONE MARROW, etc.
  • Initial cutaneous lesion may or may not be seen
  • Symptoms are though to develop months (possibly YERAS) after inoculation
  • Initial presentation –> irregular low grade fever
  • Most infections are ASYMPTOMATIC and RESOLVE
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16
Q

Leishmania spp. - Leishmaniasis (Full Blown Disease)

A

Fever, weigh loss, hepatosplenomegaly, and a WASTING appearance

  • Systemic immunosuppression is common
  • Secondary bacterial and viral infection is the typical cause of death
  • Fulminate visceral leishmaniasis typically occurs in the VERY OLD, VERY YOUNG, or MALNOURISHED

Fatal (90%) if untreated

17
Q

Leishmania spp. - Leishmaniasis (Disease Progression, Control, Treatment)

A

Only INTRACELLULAR FORMS are found in infected individuals; therefore, antibodies are of little or no protection

Resolution due to CELL-MEDIATED IMMUNITY (Gamma-interferon mediated activation of macrophages)

Control: eliminating the vector/reservoirs and interrupting transmission

Treatment: HEAVY METAL COMPOUNDS (considereable Toxicity)

18
Q

Plasmodium spp. - Malaria (Species)

A

MOST IMPORTANT of all tropical and parasitic diseases

Four Species of Plasmodium cause malaria in humans:

1) P. falciparum (causes majority and most severe cases)
2) P. vivax
3) P. malariae
4) P. ovale

Most are caused by P. falciparum and P. vivax

19
Q

Plasmodium spp. - Malaria (Life Cycle)

A

Liver Cycle followed by Bloodstream (Erythrocytic) Cycle

P. vivax and P. ovale can lie dormant in the liver as Hypnozoite for years to decades

See ANEMIA think Malaria

20
Q

Plasmodium spp. - Malaria (Malarial Paroxysm)

A

Synchronous release of merozoites and lysis of RBCs causing flu-like symptoms, including very high fever, chills, headdache, and myalgias

21
Q

Plasmodium spp. - Malaria (Duration and Pattern of Paroxysm)

A

Symptoms/Severity is dictated by species of Plasmodium involved

P. vivax and ovale recur every 48 hours
P. malariae recur every 72 hours
P. falciparum recur ever 48 hours

22
Q

Plasmodium spp. - Malaria (Malarial Paroxysm: Cold vs. Hot vs. Sweat Stage)

A

Cold Stage: (15-60 min)- rigors, cold dry skin, high core temperature, rapid pulse, nausea, vomiting

Hot Stage: (2-6 hours)- severe headache, palpitations, confusion delirium

Sweat Stage (8-12 hours)- perspiration, exhaustion, sleep

23
Q

Plasmodium spp. - Malaria (Anemia)

A

Asexual stage of parasite destroys RBCs each time it completes a cycle of replication

3 mechanisms involved in pathogenesis of anemia:

1) RBC lysis by mature asexual intra-erythrocytic parasites
2) Suppression of erythropoiesis by cytokines (TNF-a, IL-1 –> these cause fever)
3) Destruction of RBCs by the spleen

24
Q

Plasmodium spp. - Malaria (Severity)

A

Severity is dictated by species involved and population of RBCs it infects

P. falciparum –> infects both MATURE and YOUNG erythrocytes

P. vivax and P. ovale –> infect only YOUNG RBCs (reticulocytes; only about 1-3% of circulating RBCs)

  • P. vivax: can only infect reticulocytes bearing DUFFY BLOOD GROUP determinants
  • P. ovale: can infect DUFFY NEGATIVE or POSITIVE reticulocytes

P. malarie –> prefers OLDER erythrocytes

25
Q

Where is the most severe anemia commonly seen?

A

In those infected with P. falciparum; more than 20% of circulating RBCs can become infected

Other symptoms/complications:
-Splenomegaly
-Hypoglycemia/lactic acidosis - P. falciparum
-Microvascular sequestration - P. falciparum
(Cerebral Malaria –> Knobs on surface, very stick, prevent perfusion)

26
Q

Plasmodium spp. - Malaria (Diagnosis)

A

Travel history
Recognize clinical syndrome
Blood smear positive for parasites

27
Q

Plasmodium spp. - Malaria (Blood Smear)

A

Gametocytes (sexual form of parasites) seen

  • Ring Forms
  • PURPLE BANANA/CRESCENT* on blood smear is PLASMODIUM FALCIPARUM
28
Q

Plasmodium spp. - Malaria (Control, Prevention, Treatment)

A

Natural Resistance: several genetic polymorphisms that affect the properties or functions of RBCs appear to be provide some level of resistance

Control/Prevention/Treatment:

  • Eradicate insect vector/breeding grounds
  • Prophylaxis for travelers (Is it an area of chloroquine resistance? Are P. vivax or P. ovale present in this area?)
  • Vaccine trials have been disappointing
  • Drug resistance is a MAJOR CONCERN
29
Q

Babesia spp. - Babesiosis (Characteristics)

A

TICK BITE

Reservoir: Rodents (B. microti) and Cattle (B. divergens)

In US, most cases in New England, Upper Midwest, and California

OUR MALARIA - similar life cycle

30
Q

Babesia spp. - Babesiosis (Symptoms, At Risk Groups, Treatment)

A

1-8 weeks after bite –> fever, chills, myalgia, hemolytic anemia - replication of parasites in RBCs

At risk: Elderly, ASPLENIC, and immunosuppressed are at highest risk of symptomatic infection

Treatment: Atovaquone and Azithromycin (quinine/clindamycin)

MALTESE CROSS (on blood smear) —> Think Babesia spp.

31
Q

Filariasis (i.e. Lymphatic Filariasis)

A

Caused by Wuchereria bancrofti (Central Africa, Mediterranean, Asia, Indonesia, New Guinea, Caribbean, Central/South America) and Brugia malayi (Asia)

Small, thin, thread-like nematodes transmitted by the bite of MOSQUITOES

Reside in LYMPHATICS and clog them up

32
Q

Filariasis (i.e. Lymphatic Filariasis) (Life Cycle)

A
  • Transmitted by bite of infected MOSQUITOES
  • Larvae from bite wound enter the lymphatics and mature into adults (takes about 1 year)
  • This typically occurs in the lymphatics of the upper and lower extremities and male genitalia
  • Adult females release 10,000’s of microfilariae (larvae) each day, migrate from the lymphatics to the bloodstream
  • PM- large numbers (mosquito feeding)
  • AM - capillaries of the lung (results in TROPICAL PULMONARY EOSINOPHILIA –> HIGH IgE, EOSINOPHILIA, ASTHMA)

More likely to find Folaria at night

33
Q

Filariasis (i.e. Lymphatic Filariasis) (Diagnosis)

A

Observation of microfilariae in blood smears (collected at night)

34
Q

Filariasis (i.e. Lymphatic Filariasis) (Treatment)

A

DEC kills microfilarie and damages adults

Steroids are used to counteract allergic response to dying worms

Severe disease - surgery

35
Q

Schsitosoma spp. - Schistosomiasis

A 
***Flatworms (Trematodes)***
3 species:
1) S. haematobium (Bulinis)
2) S. mansoni (Biomphalaria)
3) S. japonicum (Oncomelania)

SNAILS –> Miracida penetrate our skin

Very prevalent in South America, Middle East, Asia, Philippines

36
Q

Schsitosoma spp. - Schistosomiasis (Body Sites inhabited)

A

S. mansoni - Venous plexus of LARGE INTESTINE

S. japonicum - Venous plexus of SMALL INTESTINE

S. haematobium - Venous plexus of the BLADDER (eggs in urine)

***Chronic infection results from the lodging of eggs in tissue (highly INFLAMMATORY and antigenic)

37
Q

Schsitosoma spp. - Schistosomiasis (Clinical Disease)

A

S. japonicum and S. mansoni:
-Chronic intestinal and hepatic dysfunction (portal fibrosis and portal hypertension —> LIVER FAILURE)

S. haematobium:

  • Hematuria, dysuria, urinary frequency
  • Loss of bladder function
  • Increased occurrence of SQUAMOUS CELL CARCINOMA of the bladder
38
Q

Schsitosoma spp. - Schistosomiasis (Diagnosis and Control/Prevention)

A

Diagnosis: Eggs in feces or urine

Control/Prevention:

  • Control snail population
  • Limit exposure to water
  • Improve sanitation

Microbiology Exam V (6 decks)

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