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Plasmodium falciparum Plasmodium vivax Plasmodium ovale Plasmodium malariae PowerPoint PPT Presentation


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Malaria. Plasmodium falciparum Plasmodium vivax Plasmodium ovale Plasmodium malariae. 1. Malaria geographic distribution. 2. Malaria: Case-1.

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Plasmodium falciparum Plasmodium vivax Plasmodium ovale Plasmodium malariae

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Pathmicrod sc

Malaria

  • Plasmodium falciparum

  • Plasmodium vivax

  • Plasmodium ovale

  • Plasmodium malariae

1


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Malariageographic distribution

2


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Malaria: Case-1

On January 11, 2001, a 12 year-old resident of Michigan was taken to a clinic with a 2-day history of fever with chills, malaise, fatigue, cough and one episode of vomiting.

At the clinic, the patient had a temperature of 102º F (39º C). The clinician noted that the patient had returned from Africa on January 6.

Upper respiratory tract infection was diagnosed with nausea and vomiting, and the patient was prescribed an oral cephalosporin antibiotic and antiemetic agent.

3


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Malaria: Case-1, continued

The symptoms continued and on January 14, the patient collapsed, was transported to a local hospital, and died in the emergency department shortly thereafter.

Examination of a peripheral blood film on stored blood from January 11 and a film from blood taken on January 14 demonstrated Plasmodium falciparum parasites with 0.8% parasitemia and 14 %, respectively.

The patient’s mother also had P. falciparum malaria diagnosed in January, and later recovered. Both mother and son had taken chloroquine prophylactically.

4


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Malaria: Case-2

On March 7, 2001, a 47-year-old resident of Minnesota returned to the US after 11 days in east Africa. Chloroquine was taken before and during the trip and proquanil was added on arrival in Africa.

On returning to the US, proquanil was discontinued, and on March 11, the scheduled dose of chloroquin was taken. On March 17, the patient developed a persistent headache and on March 19, sought care for headache and dark urine at a Florida hospital emergency department.

On admission, the patient’s temperature was 102º F (39º C); physical examination did not reveal any abnormalities.

5


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Malaria: Case-2, continued

A thick blood smear film obtained on admission was read as Plasmodium species, and later was confirmed as P. falciparum. The patient was admitted and treated with oral quinine and doxycycline; however, the patient developed cerebral edema and respiratory failure and died 6 days after admission.

The patient had traveled to Africa with a group of 13 person; nine had taken mefloquine for prophylaxis and four had followed the same regimen as the patient. No other malaria cases were reported from the group.

6


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Reported malaria cases in 2006

USA: 1,564 (six fatal)

South Carolina: 8

South-East:41

7


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Reported indigenous malaria cases in the US (1957-2003)

8


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Reported indigenous malaria cases in the different states (1957-2003)

9


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Species of indigenous malaria cases reported in the US (1957-2003)

10


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Malarial parasites morphology

  • Malignant tertian

  • Benign tertian

  • Ovale tertian

  • Quartan

11


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Malarial parasites life cycle

12


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type

organ Involved

symptoms

Tertian (vivax and ovale)

Headache, lassitude, vague aching of bones and joints, chills and high fever (103-106 F), nausea and vomiting, convulsion, euphoria, profuse sweating. Symptoms every other day and last 8-12 hours . Spontaneous recovery

Spleen, liver, erythrocytes

systemic

falciparum (malignant tertian)

Same as above but no tertian pattern: there may be daily spiking; no spontaneous recovery and ultimately fatal. Renal & CNS involvement

quartan (malariae)

Same as tertian, but paroxysm occurs every three days (2 clear days)

Malarial symptoms

13


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Malarial paroxysm

14


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v

f

o

m

Malarial diagnosis

  • Travel history

  • symptoms

  • Blood smear

15


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Malariacontrol and treatment

  • Control

    • Control mosquito population

    • Mosquito netting

  • Treatment:

    • Chloroquine

    • P. falciparum often drug resistant, but other drug choices are available

16


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Chloroquine: mechanism of action

Chloroquine is a 4-aminoquinoline

Inside the red blood cells malaria parasite digests hemoglobin and produces heme which is toxic to the parasite

To prevent the toxicity, parasite biocrystallizes heme to form hemozoin which is non-toxic

Chloroquine enters the red blood cells, prevents the process of biocrystallization, that leads to accumulation of heme and death of parasite

17


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Babesiosisgeography andetiology

  • Etiologic agent is Babesia microti

  • Zoonotic infection

  • Deer are primary reservoir

  • Cases reported in north-eastern part of the US and Europe

18


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Babesiosismorphology

  • Similar to malarial parasite, but no schizonts or gametocytes

  • Up to four trophozoites per cell, no sexual cycle

19


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Babesiamicrotilife cycle

20


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Babesiosissymptoms

  • Mild chills and fever

  • Hemolytic anemia

  • Jaundice

  • Hepatomegaly

    No malarial paroxysm

21


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Babesiosisdiagnosis

  • Symptoms

  • History of tick bite

    No malarial paroxysm

  • Characteristic organisms in blood

22


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Babesiosisprevention and treatment

  • Avoid tick bites

  • Recovery may be spontaneous

  • Clindamycin with quinine is effective

23


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Toxoplasmosis

  • The etiologic agent T.gondii is distributed worldwide

  • Most of the populations is seropositive

  • Threat to immunosuppressed and unborn

24


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Toxoplasmagondiimorphology

  • Intracellular (macrophage) parasite

  • 3-6 x 1-2 µm

25


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Toxoplasmagondiilife cycle

26


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host status

symptoms

Prenatal

1-5% aborted, 8-10% serious brain and eye damage, 10-13% less serious visual and mental problems, ~70% late visual and mental problems

Normal adult

Flu-like

Immuno-compromised

Parasitemia, cysts in visceral organs, eye, and CNS, often fatal

Toxoplasmosissymptoms

27


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Toxoplasmagondiiretinitis

28


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Toxoplasmagondiihydrocephalus

29


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Toxoplasmagondiiencephalitis

30


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Toxoplasma gondiiPathology and Immunology

Pathology

  • Growingmass

  • CMI

Immunology

  • Both humoral and CMI are stimulated

  • CMI is protective

31


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Toxoplasma gondiiDiagnosis and treatment

Diagnosis

  • History

  • CT scan

  • Tonsil or lymph node biopsy

Treatment

  • Sulphonamide or pyrimethamine Spiramycin

32


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Pneumocystiscarinii

Not a protozoan,

it’s a yeast

  • Opportunistic

  • Major cause of pneumonia among AIDS patients

Treatment

  • trimethoprim

  • sulphamethoxazole

33


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Facultative protozoan parasites

Negleria Fowleri

  • Rare

  • In warm spas

  • Causes encephalitis

Acanthamoeba

  • Rare

  • In soil

  • pharyngitis, occasionally encephalitis

34


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Summary of luminal and blood parasites


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Amebiasis

  • Etiologic agent:

  • Entamoeba histolytica

  • Disease:

  • Amoebic dysentery

  • Liver, lung, brain and other abscesses

1


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Fecal-oral life cycle

Excystation

Trophozoite

Cyst

Encystment

Passed in feces

Metabolically active

2


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Organ involved

Symptoms

Symptoms of acute amebiasis

Abdominal pain; frequent bloody dysentery with necrotic mucosa

Small and large intestine

3


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Organ involved

Symptoms

Symptoms of chronic amebiasis

Small and large intestine

Recurrent bloody and mucoid dysentery

Abscess; hepatitis

Liver

Abscess; pneumonia

Lung

Abscess; encephalitis

Brain

4


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E. Histolytica:pathology

Pathology

Invasiveness and abscess formation are due to amoebic proteolytic enzymes

5


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Amebiasis:Differential diagnosis

Amebiasis is different from giardiasis and bacterial dysentery

Mucus and blood in stool

No granulocytosis

No high fever

6


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E. Histolytica:the diagnostic features

When amebic dysentery is suspected, a fresh fecal sample or a swab should be examined under microscope.

If examined quickly the colorless motile trophozoite can be seen.

H/E stained

Fresh sample

7


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E. Histolytica:treatment

  • Treatment

    • Iodoquinol for acute amebiasis

    • Metronidazole for chronic amebiasis

8


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Giardiasis

  • Etiologic agent: Giardialamblia

  • Diarrhea, lipid and vitamin B12 and other nutrient mal-absorption

9


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organ involved

symptoms

stage

Acute

Small and large intestine

Flatulence; foul-smelling, bulky light diarrhea; malabsorption, lactose intolerance

Chronic

Small and large Intestine

Asymptomatic or symptoms described above

Giardiasis:

symptoms

10


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Giardiasis: pathology

Pathology

  • Covering of the epithelium by trophozoites and flattening of the mucosal surface (no invasiveness)

11


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Giardiasis:

Differential diagnosis

Giardiasis is different from amebiasis and bacterial dysentery:

No mucus, blood

No granulocytosis and no fever

12


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Giardiasis:

diagnosis

The mainstay of diagnosis of Giardia is stool microscopy, this can be for distinctive oval cyst and motile trophozoite

13


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Giardiasis: treatment

  • Treatment

    • Iodoquinol

    • Metronidazole

14


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Balantidium coli

  • Primarily a zoonotic intestinal parasite:

    • Horses, cows, pigs

  • Farm workers at risk

  • Symptoms similar to amebiasis except,

    No abscesses in peripheral organs

15


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Balantidium coliDiagnosis

History, symptoms and finding the typical trophozoites and cysts in the stool

16


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Balantidium coliPrevention and treatment

Prevention

Avoid ingestion of material contaminated with animal feces

Treatment

Tetracycline

Iodoquinol

Metronidazole

17


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Cryptosporidium parvum

Major cause of epidemic/community diarrhea

Animal reservoir (domestic animals)

Severe diarrhea and invasive infection in AIDS patients

18


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Cryptosporidium parvum

Cryptosporidium is typically a acute short term infection. The parasite is transmitted by oocysts that, once infected, excyst in the small intestine.

19


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Cryptosporidium parvumTreatment and control

  • Self limiting in normal individuals

  • Severe and prolonged disease in AIDS patients

  • Nitazoxanide

  • Proper sanitation and clean water supply

20


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Isospora belli

  • Causes giardiasis-like but milder symptoms

  • Self limiting in normal individuals

  • Severe and prolonged disease in AIDS patients

  • Multiplies both sexually and asexually

21


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Isospora belli

  • Diagnostic stage of I. Belli in fresh stool oocyst with 1 sporocysts

  • Treatment:

    TrimethoprimSulphamethoxazole

Microscopic demonstration of the oocysts with one sporocyst.

22


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Trichomonasvaginalismorphology

  • Human parasite only

  • There is no cyst in the life cycle, transmission is via trophozoite stage

  • World-wide

    • 5% in normal population

    • 70% among prostitutes and female prison inmates

23


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TrichomonasvaginalisSymptoms

Women

Often asymptomatic

Mild to severe vaginitis in heavy infections

Copious fowl-smelling yellow discharge

Growth of the organism favored by high pH: >5.9 (N=3.5-4.5)

24


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TrichomonasvaginalisDiagnosis

Giemsa stained T. vaginalis (vaginal swab)

25


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TrichomonasvaginalisPrevention Treatment

  • Prevention:

    • Personal hygiene

    • Condom use

  • Treatment

    • Metronidazole

    • Vinegar douche (decreases pH)

26


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Metronidazole: Mechanism of action-

Metronidazole is nitroimidazole compound

Pfizer markets the drug under the trade name Flagyl

Metronidazole is a prodrug. The nitro group of the compound is reduced by ferredoxin and the resulting products are responsible for disrupting the DNA helical structure which leads to inhibition of nucleic acid synthesis

27


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Trypanosomabruceimorphological forms

Epimastigote (crithidial form) in the insect

Trypomastigote (trypanosomal form) in the mammalian host

28


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 stage

organ Involved

symptoms

Bite reaction

Skin

Painful chancre; no scar

Parasitemia

Blood circulation and lymph nodes

Fever, edema, lymphadenopathy

Tremulous speech, mental retardation, sleepiness, cardiac failure.

CNS (T. gambiense)

Heart (T. rhodesiense)

CNS stage

Trypanosomiasis symptoms

29


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T. Brucei :Winterbottom’s sign

30


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T. Brucei : pathology and Immunology

Pathology

  • Inflammation

  • Antigenic change

  • CNS damage by the organisms

31


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T. Brucei :diagnosis

  • History of travel and Tsetse fly-bite

  • Symptoms

  • Blood smear and/or CSF

32


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T. Brucei : Treatment

  • Acute disease

    • Suramin

    • Pentamidine

  • Chronic (CNS) disease

    • Melarsoperol (arsenic)

33


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American trypanosomiasisEtiologic agent (T. cruzi)

34


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stage

symptoms

organ involved

Primary lesion

Nonpurulent edematous plaques

Skin

Hepatomegaly, splenomegaly, acute myocarditis, generalized edema

Acute stage

Lymph node and heart

Chronic stage

Hollow organs

Mega esophagus, mega colon, cardiomegaly, cardiac arrhythmia

Chagas’ disease (T. cruzi) :

symptoms

35


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  • Bioassay in mice or uninfected triatoma

36


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  • Nifurtimox effective in acute stage

  • Benznidazole may be of value in chronic stage

  • Avoid and control the insect population

  • No vaccine

37


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Organism

Disease

Epidemiology

L. donovani

Asia: 10x106

visceral leishmaniasis

L. tropica

cutaneous leishmaniasis

Mediterranean: 5x106

L. Braziliensis and other

mucocutaneous leishmaniasis

South/Central America: 10x106

38


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Leishmaniamorphology

  • Amastigote (leishmania) seen in the mammalian host

  • Promastigote (leptomonad) seen in sand fly

39


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Type

Organ Involved

Symptoms

Visceral

Liver, spleen, bone marrow, lymph nodes, skin

No bite reaction; lymphadenopathy, splenomegaly and hepatomegaly; parasitemia, chills and fever; darkening of skin

Cutaneous

Skin

Centrifugally growing papular lesion with central crusting; permanent scar

Muco-cutaneous

Skin and mucoid tissue

Necrosis of mucoid tissue; metastasis to distant mucoid tissues; very disfiguring

40


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Leishmania: Diagnosis

  • History

  • Lesions or symptoms

  • Organisms in the lesion

  • Montenegro test

    (type IV hypersensitivity)

41


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LeishmaniasisPreventions and treatment

  • No vaccine

  • Control of sand fly and infected animals

  • avoidance of sand fly

  • Pentosam (antimony gluconate)

42


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Malarial parasites morphology

  • Malignant tertian

  • Benign tertian

  • Ovale tertian

  • Quartan

43


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Malarial parasites life cycle

44


Pathmicrod sc

Type

Organ Involved

Symptoms

Tertian (vivax and ovale)

Headache, chills and high fever (103-106 F), profuse sweating. Symptoms every other day and last 8-12 hours . Spontaneous recovery

spleen, liver, erythrocytes

systemic

Falciparum (malignant tertian)

Same as above but no tertian pattern: there may be daily spiking; no spontaneous recovery and ultimately fatal. Renal & CNS involvement

Quartan (malariae)

Same as tertian, but paroxysm occurs every three days (2 clear days)

Malarial symptoms

45


Pathmicrod sc

v

f

o

m

Malarial diagnosis

  • Travel history

  • symptoms

  • Blood smear

46


Pathmicrod sc

Malariacontrol and treatment

  • Control

    • Control mosquito population

    • Mosquito netting

  • Treatment:

    • Chloroquine

    • P. falciparum often drug resistant, but other drug choices are available

47


Pathmicrod sc

Babesiosisgeography andetiology

  • Etiologic agent is Babesia microti

  • Zoonotic infection

  • Deer are primary reservoir

  • Cases reported in north-eastern part of the US and Europe

48


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Babesiosismorphology

  • Similar to malarial parasite, but no schizonts or gametocytes

  • Up to four trophozoites per cell, no sexual cycle

49


Pathmicrod sc

Babesiosissymptoms

  • Mild chills and fever

  • Hemolytic anemia

  • Jaundice

  • Hepatomegaly

    No malarial paroxysm

50


Pathmicrod sc

Babesiosisprevention and treatment

  • Avoid tick bites

  • Recovery may be spontaneous

  • Clindamycin with quinine is effective

51


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Toxoplasmagondiimorphology

  • Intracellular (macrophage) parasite

  • 3-6 x 1-2 µm

52


Pathmicrod sc

host status

symptoms

Prenatal

1-5% aborted, 8-10% serious brain and eye damage, 10-13% less serious visual and mental problems, ~70% late visual and mental problems

Normal adult

Flue-like

Immuno-compromised

Parasitemia, cysts in visceral organs, eye, and CNS, often fatal

Toxoplasmosissymptoms


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Toxoplasmagondiilife cycle

53


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Toxoplasmagondii: treatment

  • Treatment

  • Sulphonamide or

  • Spiramycin

55


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