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Block 7 week 4 > Schistosomiasis and Malaria - Hunter > Flashcards

Schistosomiasis and Malaria - Hunter Flashcards

1
Q

What are the major species of Schistosoma?

A
  1. S. mansoni
  2. S. haematobium
  3. S. japonicum
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2
Q

What are the minor species of Schistosoma?

A
  1. S. mekongi

2. S. intercalatum

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3
Q

What is the geographic distribution of S. mansion and S. intercalactum?

A

Mainly SubSaharan Africa, small parts of Puerto Rico, and the Carribean Islands and some coastal areas of Brazil.

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4
Q

What is the geographic distribution of S. haematobium, S. japonicum and S. mekongi?

A
  1. S. haematobium - Sub Sahran Africa
  2. S. japonicum - isolated spots of China and the phillipines
  3. S. mekongi - Mekong region of Vietnam
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5
Q

Describe the lifecycle of S. mansoni.

A
  1. cercaria comes into contact with human skin in water and penetrates to gain access to body
  2. cercaria loses tail and becomes a schistosomule
  3. schistosomule travels to lungs via blood stream and hangs out until it gets directional signal, then it goes to the mesenteric veins gains access to portal circulation and hangs out by the liver for awhile before going back to the mesenteric veins where the adult form attaches
  4. male and female mate here - they mate continuously and occasionally the female detaches from the male and releases eggs
  5. eggs have enzymes to erode tissue to gain access to the lumen of large intestine where they are passed with feces
  6. eggs hatch when they hit water - mericidium form emerges
  7. mericidium seeks its specific species of aquatic snail and undergoes asexual reproduction
  8. cercaria emerge from snails and must find human host or monkey in a short time
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6
Q

What is the infective form of Schistosoma?

A

The cercaria.

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7
Q

What is the intermediate host of the Schistosoma?

A
  1. S. mansoni - snail genus Biomphalaria
  2. S. haematobium - snail genus Bulinus
  3. S. japonicum - snail genus Oncomelania
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8
Q

What must happen in order for a person to be infected by Schistosoma?

A

At least one male and one female must gain access to the human host. Females live inside a pouch in the male - they attach this way to copulate. The male has ‘suckers’ that allow him to attach to mesenteric veins.

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9
Q

How does a cercaria find a human host?

A

They can sense amino acids released from human skin into water.

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10
Q

What allows the adult worms to evade the human immune system?

A

The skin of the adult worms acquires host molecules such as host glycoproteins and host MHC molecules - this allows them to to be immunologically disguised.

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11
Q

Which form of the parasite causes human pathology?

A

The eggs cause pathology due to their enzymes that erode host tissue. Also the egg and its protein products are highly antigenic and produce significant immune response. The adults don’t really cause pathology.

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12
Q

What is the reservoir for S. mansion?

A

A monkey.

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13
Q

What can cercarial penetration cause?

A

Transient dermatitis.

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14
Q

What can migration of schistosomules cause?

A

Migration through the lung can cause pneumonitis - more severe in heavy infections.

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15
Q

Describe some other clinical pathologies caused by Schistosomas.

A
  1. onset of egg production can cause an allergic response called Katayama fever that can be fatal
  2. in S. japonicum and S. mansoni infections egg travel through the bowel causes bloody diarrhea and gastroenteritis
  3. in S. hematobium infections egg travel through the bladder wall causes hematuria and hemorrhagic cystitis
  4. in chronic infections eggs passing through the bladder and bowel cause fibrosis of the tissue and then eggs have a harder time passing through and some get back into circulation
  5. if eggs get into portal circulation some can cause granuloma formation in the liver
  6. blockage of liver sinusoids leads to pipestem fibrosis and portal hypertension
  7. clincial and lab findings may include hepatosplenomegaly, hyperimmunoglobulinemia and eosinophilia
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16
Q

Where do adult S. mansion worms attach?

A

They prefer mesenteric veins of the large intestines.

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17
Q

Where do adult S. japonicum worms attach?

A

They prefer mesenteric veins of the small intestines.

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18
Q

Where do adult S. hematobium worms attach?

A

They prefer the vesicle plexus of the bladder.

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19
Q

Do adult worms cause pathology?

A

No.

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20
Q

What happens if Schistosoma eggs get into portal circulation?

A
  1. the eggs are large and they block sinusoids and get stuck there
  2. they cause a T cell mediated type IV hypersensitivity reaction leading to formation of granulomas
  3. blockage of sinusoids and granulomas lead to pipestem fibrosis and portal hypertension
  4. portal Hypertension causes ascites
  5. the eggs can also get into other tissues such as the kidneys and the brain
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21
Q

What types of cellular infiltrates will you see when eggs travel through host mucosa of the intestines or bladder?

A
  1. initially there will be a infiltration of neutrophils - indicates acute inflammation
  2. eventually there will be an infiltration of mononuclear cells - indicating chronic inflammation
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22
Q

What types of cell swill you see in granulomas of the liver?

A
  1. T cells
  2. giant cells
  3. epitheliod cells
  4. if there are many granulomas this could lead to fibrosis and liver failure
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23
Q

What is the main difference between S. mansoni eggs and S. japonicum eggs?

A

S. japonicum eggs are much smaller. Because they are smaller the eggs are more likely to get through the portal circulation and get into other tissues such as the lungs and cause pathology.

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24
Q

The egg of which species of Schistosoma has a terminal spine?

A

S. hematobium.

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25
Q

The egg of which species of Schistosoma has a lateral spine?

A

S. mansoni. Also S. japonicum, but the spine and the egg itself is much smaller than that produced by S. mansoni.

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26
Q

What is a concern in endemic areas where schistosomiasis is chronic?

A

Chronic infection and large worm burdens cause a disruption in the normal development of children.

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27
Q

What drug is used to treat Schistosomiasis?

A

Praziquantel - this drug kills the adult worm and prevents the production of eggs.

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28
Q

What form of the Schistosoma parasite does the human immune system act against?

A

The host immune system forms IgM antibodies against schistosomules. IgM is switched to IgE and IgE works with eosinophils to try to clear infection. Eosinophils are unable to phagocytize the schistosomule because they are too large - instead it releases anti-worm enzymes from granules.

29
Q

Describe the epidemiology of Malaria.

A
  1. 300-500 million cases globally each year
  2. 90% of cases occur in Africa
  3. endemic to more than 90 countries
  4. 40% of world population at risk
  5. 10% of world population gets sick each year with malaria
30
Q

What is the most common age of death by malaria?

A

4 years old - every 30 seconds a child dies of malaria - 3000 per day and up to 23% of African infants are born with the parasite.

31
Q

Are malaria cases seen in the US?

A

Yes, there are some but they are imported cases.

32
Q

Name the four malarial parasites.

A
  1. Plasmodium vivax
  2. Plasmodium ovale
  3. Plasmodium malariae
  4. Plasmodium falciparum
33
Q

What is the geographic distribution of malaria?

A
  1. Mainly Sub Saharan Africa

2. Also seen in China, India, the Middle East, South America and Central America

34
Q

Describe the life cycle of the malaria parasite in humans.

A
  1. female Anopholes mosquito bites human and injects sporozoites
  2. sporozoites travel to the Liver and undergo asexual reproduction in schizont in hepatocyte to form merozoites - no pathology associated with this
  3. hepatocytes rupture and release merozoites into blood where they invade RBC’s and reproduce
  4. RBC’s rupture - leading to cyclical nature of symptoms - and parasite enters a new RBC…….
  5. Some parasites will become male and female gametocytes
  6. gametocytes are picked up by a female Anopholes mosquito when she bites and infected human
35
Q

What is the life cycle of the malaria parasite in the mosquito?

A

Once in the mosquito, the male gametocyte will exflaggelate and release gametes that will fertilize a female gametocyte and a zygote is formed. The zygote will attach to the wall of the mosquito gut and will form an oocyte in which sporozoites will form. The oocyte ruptures, releasing sporozoites that have a tropism for the salivary gland of the mosquito. When the mosquito bites a person the sporozoites will be injected.

36
Q

What is the infective form of the parasite for humans?

A

The sporozoite. The mosquito is driven to bite a person because she must have a blood meal to form eggs. The sporozoites are injected from her salivary gland into the person when she bites.

37
Q

What is the leading cause of sepsis and septic schock in the world?

A

Malaria.

38
Q

What form of the malaria parasite is the erythrocytic form or the one that infects RBCs?

A

The merozoite is the form. They have specific structures that allow them to bind to an RBC and get inside without rupturing it. Once inside the change, grow and multiply. They consume the globin part of hemoglobin and leave a black pigment called hemozoin. The manifestations of malaria are caused by the merozoites.

39
Q

Why is malaria a systemic inflammatory disease?

A

It causes massive release of TNF-a and other pro-inflammatory and pyrogenic cyokines.

40
Q

What is the classical fever paroxysm associated with malaria?

A

It refers to the cyclical nature of fever associated with malaria - this corresponds to synchronized rupture of erythrocytes.

41
Q

Describe the timing of the fevers caused by the different parasites.

A
  1. P. falciparum - also called malignant tertian - there is no real synchronization of RBC rupture so fever is continuous
  2. P. vivax - also called benign tertian - rupture and fever every other day
  3. P. ovale - also called oval tertian - rupture and fever occur every other day
  4. P. malariae - also called quartan malaria - rupture and fever occur every third day
42
Q

What are some important clinical and lab findings of malaria?

A
  1. anemia
  2. hepatosplenomegaly
  3. hyperimmunoglobulinemia
43
Q

What are some disease sequellae of malaria and why?

A

Immune complexes are formed so malaria can lead to glomerulonephritis, nephrosis, and cerebral malaria. Most organ systems are affected by malaria.

44
Q

Which two species have a form of parasite that can cause relapse?

A

P. vivax and P. oval leave a form in the liver called a hypnozoite. This form can cause relapse.

45
Q

What two forms of the malaria parasite recrudesce intend of cause relapse?

A

P. falciparum and P. malariae. Basically these two can lead to subclinical infection. Sometimes the subclinical infections can become active clinical disease.

46
Q

Which malarial species is almost always associated with cerebral malaria?

A

P. falciparum.

47
Q

Describe Malarial Rigor.

A

This basically occurs when RBCs rupture and inflammation is taking place.

  1. cytokines and parasite pyrogens act on the hypothalamus to reset the hypothalamic set point for body temperature
  2. body temp increases and there is peripheral vasoconstriction
  3. vasoconstriction causes chills and muscle shakes - ‘Cold’ stage
  4. fever follows - ‘Hot’ stage
  5. when fever breaks there is massive sweating - Diaphoresis stage
48
Q

What are some clinical complications of P. falciparum malaria?

A
  1. cerebral coma
  2. anemia
  3. pulmonary edema
  4. renal failure
  5. shock
  6. lactic acidosis
  7. hypoglycemia
  8. tropical splenomegaly
  9. if pregnant - can cause maternal death, stillbirth, low birth weight and anemia
49
Q

What are some clinical complications of P. vivax and P. oval?

A
  1. splenic rupture
  2. anemia
  3. debilitating fevers
  4. higher TNF-a per parasite
50
Q

What are some clinical complications especially associated with P. malariae.

A
  1. immune complex formation

2. glomerulonephritis leading to nephrotic syndrome

51
Q

Describe how P. falciparum infection is treated.

A
  1. transfer severely ill patients to ICU and make rapid clinical assessment including measurement of blood glucose
  2. initiate antimalarial chemotherapy using optimal doses of appropriate agent - IV - using a loading dose
  3. monitor clinical and parasitologic responses
  4. prevent, or treat early the numerous complications - especially seizures, hypoglycemia, hyperpyrexia, and secondary infections
  5. ensure correct fluid, electrolyte and acid-base balance. control fluid replacement to prevent circulatory overload and pulmonary edema. anticipate renal and respiratory failure
  6. expert nursing care of the unconscious patient is essential
  7. avoid the use of potentially harmful ancillary treatments of unproven benefit such as corticosteroids, heparin and epinephrine
52
Q

Immune complexes can be formed in malaria. They can go to kidney and cause damage but where else might they become sequestered?

A

They can become sequestered in vasculature and cause hemorrhages.

53
Q

How can infection of an RBC by malaria parasite effect its morphology?

A

Parasites in infected cells excrete a substance that can show up on the surface of the RBC - called plasmodium falciparum erythrocyte membrane protein 1. This substance can bind to adhesion receptors in deep vasculature. If they bind to deep vascualture in the brain then they can cause cerebral malaria.

54
Q

What is cerebral malaria?

A

When infected RBC’s bind to deep vasculature in the brain and cause encephalopathy and seizure. There is a greater than 90% fatality rate with cerebral malaria.

55
Q

How is malaria diagnosed?

A

If clinically suspected then can take a thick blood film to look for parasite and a thin blood film to distinguish which species is present. There are also rapid immunoassay kits available.

56
Q

How is a thick blood film made?

A
  1. put a thick drop of blood on a slide and let it dry
  2. put the slide in water so that the RBCs will rupture
  3. the parasite is left behind
57
Q

On a thin film with P. vivax what characteristics are diagnostic?

A
  1. infected RBCs are larger than normal ones
  2. there will be stippling on the surface of the cell
  3. there will be large numbers - greater than 20 per cell - of active ameboid merozoites in a schizont
58
Q

On a thin film with P. ovale what characteristics are diagnostic?

A
  1. RBC will have oval shape
  2. there will be stippling on surface of cell
  3. will have less merozoites per schizont than vivax
59
Q

On a thin film with P. malariae what characteristics are diagnostic?

A
  1. RBCs will have 12 or less merozoites in schizont

2. will see lots of malaria pigment

60
Q

On a thin film with P. falciparum what characteristics are diagnostic?

A
  1. look for signet ring appearance

2. look for banana shaped gametocytes

61
Q

Can there be infections with more than one species at one time?

A

Yes.

62
Q

Describe some genetic factors that are associated with malaria.

A
  1. Host RBCs do not have MHC molecules so once the parasite is inside they are invisible to the immune system
  2. the parasite can change its properties - can undergo antigenic variation to evade immune response
  3. the malarial parasite turns on B cells non-specifically in the spleen so that there will be an enlarged spleen with lots of B cells that are proliferating and making antibodies - but not antibodies to the parasite - this is a defense mechanism of the parasite
  4. acquired immunity is a complex interaction of cell mediated and humoral immune mechanisms - immunity is species, strain and stage specific
63
Q

What are some ways that people in endemic areas have evolved to prevent infection with the malarial parasite?

A
  1. In West Africa - susceptibility to vivax malaria is determined by the presence of absence of the Duffy blood group receptor - this is the receptor on the outside of the RBC that vivax parasites bind to in order to get in the RBC
  2. Individuals who are heterozygous for sickle cell disease are protected - The parasites do not like to consume HbS
  3. In West Africa - if an individual has the HLA-B53 allele they are protected - this allele carries a gene for anti-malaria peptide that allows the person to mount a T cell response to the parasite
64
Q

What are the drugs that can kill erythrocytic forms of the malaria parasite?

A
  1. artemisinin and artemisinin combined therapy
  2. chloroquine
  3. doxyclycline
  4. halofantrine
  5. quinidine
  6. quinine
  7. mefloquine
  8. proguanil
  9. pyrimethamine-sulfadoxine
65
Q

What drug can kill the hepatic form (hypnozoite) of the malaria parasite?

A

Primaquine. This drug would be given if infection involved the ovale or vivax parasites which have a hypnozoite form. This drug is contraindicated in patients with G6PD deficiency.

66
Q

What is a major problem with chemotherapy for malaria?

A

Drug resistance is widespread - particularly chloroquine resistance.

67
Q

What would you take if you were going to travel to a country where malaria is endemic?

A

There is no vaccine to malaria so chemoprophylaxis is the treatment of choice. The choice of drug is dependent on the resistance in the particular area the person is going to.

68
Q

Worldwide, malaria eradication programs have failed. What are some reasons that contributed to the failure?

A
  1. the emergence of drug resistant parasites
  2. widespread mosquito resistance to DDT and other insecticides
  3. wars and massive population movements
  4. corrupt governments
  5. difficulties in obtaining sustained funding from donor countries
  6. lack of community participation and education in host countries

Block 7 week 4 (6 decks)

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