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DTM&H > Haemoflagellates > Flashcards

Haemoflagellates Flashcards

1
Q

What organism family is responsible for leishmaniasis?

A

Leishmania spp.

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2
Q

What vector is associated with leishmaniasis?

A

Phlebotomine Sandfly (old World)
Lutzomyia (new world)

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3
Q

What is the life cycle of Leishmania?

A
  1. Promastigotes injected into skin by the sandflies enter into macrophages and other phagocytic immune cells (Remember P for enter into Phagocytic cells)
  2. Within macrophages, they transform in AMASTIGOTES
  3. AMASTIGOTES undergo simple division and can infect more phagocytic cells and continue the process, or can be ingested by sandflies to spread more infection
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4
Q

Which populations are most at risk for Leishmaniasis?

A

Refugees and displaced people
Malnourished
Children > adults
HIV +ve and immunocompromised

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5
Q

What is the global burden of Leishmaniasis?

A

12 million cases in total
2 million new cases per year

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6
Q

Leishmaniasis can be grouped into OLD WORLD vectors and NEW WORLD species.

With this in mind, what is the epidemiology of Cutaneous Leishmaniasis?

A

Most common form of Leish.

95% of cases occur in:
Americas
Mediterranean Basin
Middle East
Central Asia

Current outbreak in Syria, spurred by conflict

Not especially found in SSA

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7
Q

Which Species of Leishmania are associated with Cutaneous Leishmaniasis?

A

There are NEW WORLD and OLD WORLD spp. associated with CL.

NEW WORLD:
- mexicana
-venezuelensis
-amazonensis
- braziliensis (assocaited with MCL)

OLD WORLD:
- major
- tropica
- ethiopica

  • infantum
  • donovani
    (these latter two are also implicated in VL)

(EMTs drive you in a VAM)

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8
Q

Leishmaniasis can be grouped into OLD WORLD vectors and NEW WORLD species.

With this in mind, what is the epidemiology of muco-cutaneous Leishmaniasis?

A

90% of cases occur in Bolivia

Other:
Ethiopia
Peru
Brazil

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9
Q

Which organism is especially linked with MCL?

A

L. Braziliensis

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10
Q

What spp. is especially linked with DCL?

A

L. aethiopica

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11
Q

What species of leishmania are associated with mucocutaenous Leish?

A

Peruana
Panamanis
Guyanensis
Brazilensis

**Brazilensis is the main one tho

(I have no way to remember this. Just know your Central/SA geography i guess. you could probably guess any SA country on the exam and be correct) ha

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12
Q

what is the epidemiology of visceral leishmaniasis?

A

90% of cases occur in:
Brazil, China, Ethiopia, Eritrea, India, Kenya, Somalia, South Sudan, Sudan and Yemen.

** Bahir India is the main global focal point of VL and has the highest rates of PKDL

(Almost all of these are in the ‘Old World’)

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13
Q

What main spp. of Leishmania are associated with Visceral Leish?

A

Donovani
Infantum
Chagasi

(How to remember? Visceral Leish is a DIC)

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14
Q

what main spp. of leishmaniasis is most assocaited with PKDL?

A

L. donovani

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15
Q

Is VL anthroponotic (human - human) or zoonotic (animal - human)

A

BOTH

Anthroponotic: India, Asia
Zoonotic: Europe and Mediterranean Basin, Americas (Canine and rodent vectors)

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16
Q

What are the most common disease syndromes of Leishmaniasis?

A

Cutaneous
Diffuse Cutaneous
Mucocutaneous
Visceral

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17
Q

What is the presentation of Cutaneous Leish?

A

Ulcerating skin lesion (painless)
Can be Wet (raised edge) or Dry (scab-like appearance)
Can spread along lymphatics and cause DCL

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18
Q

What is the presentation of MCL?

A

Ulcerating lesion in the naso-oral mucosa

Rarely spontaneously cured

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19
Q

What is the incubation of VL?

A

1 month up to 10 years

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20
Q

How does VL present?

A

Low grade fever
Progressive hepatosplenomegaly
Anaemia
Wasting
Intercurrent infections (from huge destruction of phagocytic cells)

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21
Q

What are complications of VL?

A

Post Kala-Azar Dermal Leish (PKDL)
Death
Splenic infarcts
Infection
Anaemia
Wasting
Malnutrition

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22
Q

What is the epidemiology of PKDL?

A

Sudan (>60% of cases)
India

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23
Q

How do you diagnose CL/MCL/DCL?

A

Skin scraping/skin snip/aspirate
- impression smear
- histology
- culture

PCR

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24
Q

How do you diagnose VL?

A

Liver/Spleen/Bone marrow biopsy
- impression smear
- culture
- histology

Serology
- rk39 antigen (urine)
- DAT
- ICT

PCR

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25
Q

What is in your differential for CL/DCL?

A

Staph infection
Buruli ulcer
Leprosy
BCC
Myiasis

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26
Q

How do you manage CL/MCL/DCL?

A

Many options:
SSG 20mg/kg for 10/7

Intralesional pentivalent antimony (for example SSG)

Miltefosine

Liposomal Amp B

Parmomycin

Note: the treatment is really complicated, and I would look at the local guidelines rather than memorising everything

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27
Q

How do you manage VL?

A
  1. Liposomal Amp B
  2. Amphotericin B
  3. Miltefosine
    3b. Paromomycin
  4. Pentavelent Antimony (e.g. SSG)
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28
Q

What is the prognosis of VL?

A

90% mortality rate if untreated

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29
Q

How can you prevent Leishmaniasis?

A

Personal precautions :
avoid sandflies
keep skin covered
use insect repellent
use impregnated clothing + bed nets

Control measures :
survey + control vector population
survey + control reservoir host populations

Medical intervention :
inoculation against CL tried in some countries
early recognition (briefings + warning cards)
early + appropriate referral to a specialist
clinical guidelines (published) + regular audit

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30
Q

What organism causes Chagas Disease

A

Trypanosoma Cruzi

31
Q

What is the vector for American Trypanosomiasis?

A

Triatomine bug of the Reduviid family

32
Q

How can American trypanosomiasis spread?

A

Vector
Blood transfusion
Vertical transmission
Transplant
Acai Juice
Sugarcane

33
Q

What is the epidemiology of Chagas Disease

A

South and Central America
12 million people currently infected

**patients can be found all over the world due to immigration

34
Q

What is the lifecycle of Chagas Disease?

A
  1. Metacyclic trypomastigotes are excreted by a feeding Reduviid bug. They enter into the skin through the feed site, or through nearby membranes (e.g. conjunctiva)
  2. Metacyclic tryps enter into various tissues, where they enter into cells and develop into amstigotes
  3. Amastigotes replicate through binary fission, creating trypomastigotes.
  4. These trypomastigotes then go to other sites, where they can cause disease, or mature into amastigotes to perpetuate further infection
  5. Trypomastigotes are taken up by a Reduviid bug
  6. They develop into epimastigotes (binary fission) –> metcyclic tryps all in the mid and hind gut, ready to infect the next victim
35
Q

How does Chagas Disease present?

A

ACUTE:
Most cases are asymptomatic; only 1-2% of cases are diagnosed here
- Chagoma at bite site
- Romañas sign
- Fever
- Lymphadenopathy
- Hepatosplenomegaly

CHRONIC:
5-10 years after initial infection
Cardiac dysfxn: palpitations, syncope, RBBB –> Complete HB

COMPLICATIONS:
- Cardiomegaly
- Megacolon
- Megaoesophagus

36
Q

How do patients with HIV Co-infection present with Chagas?

A

Meningoencephalitis
SOL which appears similar to toxo

37
Q

How do transplant patients (or people who received Chagas secondary to transplant) present?

A

Fever
Rash
Myocarditis

38
Q

How do you diagnose Chagas?

A

ACUTE:
- Blood Film - Trypomastigotes
- Tissue biopsy - amastigotes

ACUTE/CHRONIC:
- Serology (ideally x2 different tests, e.g. ELISA + one other)

IF serology is POSITIVE…
PCR

If serology is negative then presume the diagnosis is not Chagas

39
Q

What is the management of Chagas in acute illness?

A

Benzimidazole

or

Nifurtimox

40
Q

What is the management of Chagas in establish disease?

A

End organ dysfxn management (i.e. cardiac pacemaker etc.)

**At this stage of disease anti-parasitic agents are not useful and the risk of side effects are too great

41
Q

What is the treatment of Chagas in pregnant women?

A
  • Benzimidazole/nifurtimox are contraindicated in pregnancy
  • HOWEVER Chagas does spread vertically so:
  • antenatal screening of high-risk pregnancies is important; if a woman is positive do not treat while pregnant, but give meds to baby when they are born
42
Q

What organism causes Human African Trypanosomiasis?

A

Trypanosoma Brucei Rhodensi
Trypanosoma Brucei Gambiense

43
Q

What is the epidemiology of T. b. rhodensi?

A

East Africa
- Savannah habitats
- anthroponotic only

44
Q

Who is most at risk of T. b. rhodesiense?

A

It is a zoonotic spp, and the tsetse flies feed on dead game animals

  • hunters
  • honey gatherers
  • firewood gatherers
  • fishermen
45
Q

What is the epidemiology of T. b. gambiense

A

West and central Africa, especially DRC

90-98% of HAT cases

non-zoonotic, human to human transmission only

Common around rivers

Generally, incidence and prevalence decreasing due to increased Test and Treat programmes

46
Q

What vector causes African Sleeping Sickness?

A

Tsetse fly (Glossina Spp.)

47
Q

What is the lifecycle of Trypanosoma Brucei?

A
  1. Tsetse fly injects person with metacyclic trypomastigotes
  2. Metacyclic trypomastigotes enter into lymphatics and shed their tail, becoming trypomastigotes
  3. Trypomastigotes enter into blood where they cause the haemolymphatic stage of infection (long form of trypomastigote)
  4. They enter into the CNS and become the short form of trypomastigotes, replicating through binary fission. At this stage they can cross the BBB
  5. Trypomastigotes (short form) are taken up by the Tsetse fly (glossina spp) at the next feed
  6. Within the gut of the tsetse fly they transform into procyclic trypomastigotes
  7. Procyclic –> epimastigotes in the salivary glands
48
Q

What are the two stages of HAT spread?

A
  1. Haemolymphatic spread
    - trypomastigotes that were in injected in the blood multiple in the tissues, blood and lymph
  2. Neurological spread
    - trypomastigotes cross the BBB and invade neurological tissue –> altered sleep cycle,

±3. Severe Neurological spread (>100WCC on CSF + Tryps seen on CSF)

49
Q

How does HAT present?

A

HAEMOLYMPHATIC STAGE
chancre at bite site
headache, fever, weakness, joint and muscle pain
lymphadenopathy (Winterbottom’s sign)
Intermittent fever over the course of several months

CNS Stage:
sleep disorders, deep sensory
disturbances, abnormal tone and mobility, ataxia, psychiatric disorders, seizures, coma, death (if untreated)

50
Q

Which T. Brucei presents slowly?

Which presents quickly? .

A

Gambiense is slow presenting

Rhodesiense is Rapid onset (re: R for Rhodesiense)

51
Q

How is HAT diagnosed?

A
  1. Evidence of Trypomastigotes in blood, lymhc aspirate or CSF
    - Complete CSF in all patients with ME signs
    - <5 WCC and no Tryps: Haemolymphatic stage
    - >5 WCC on CSF +/- tryps is moderate
    ->100 WCC on CSF and tryps is severe disease
    NB: all patients with suspected HAT need an LP because it guides your Rx.
  2. Serum: Anti-trypomastigote antibodies
  3. CATT (T.b. gambiense only)
  4. RDT (T.b gambiense only)
52
Q

How is T. b. gambiense managed?

A

STAGE 1: Pentamidine
OR
Fexinidazole

STAGE 2: Elflornithine
OR
Nifurtimox/Elflornithine combo therapy (NECT)
OR
Fexinidazole

OR another way of writing it:

For patients aged ≥ 6 years and body weight ≥ 20 kg:
ƒ < 100 WBC/μL CSF –> fexinidazole
ƒ ≥ 100 WBC/μL CSF –> NECT
ƒ CSF WBC not available –> NECT

For patients aged < 6 years or body weight < 20 kg:
ƒ ≤5 WBC/μL CSF, no trypanosomes –> pentamidine
ƒ > 5 WBC/μL CSF or trypanosomes –> NECT
ƒ CSF WBC not available –> NECT.

Fexinidazole is therefore the first-choice treatment in patients aged ≥ 6 years and body
weight ≥ 20 kg presenting without clinical features consistent with severe meningo-
encephalitic HAT or presenting with < 100 WBC/μL in CSF. It is recommended that
fexinidazole be prescribed only when there is high confidence that the patient will have
appropriate follow-up to detect relapse early.

53
Q

How is T. B. Rhodesiense managed?

A

STAGE 1: Suramin
OR
Pentamidine

STAGE 2: Melarsoprol

54
Q

Which two drugs can be used in T b. Rhodesnsei and Gambiense?

A

Melarsoprol
Pentamidine

55
Q

In which patient population is fexanidazole contraindicated?

A

A patient aged < 6 years or body weight < 20 kg (i.e. a patient for whom fexinidazole is
not indicated) must undergo a lumbar puncture and a CSF examination to determine the
treatment choice.

NOTE: Safe to use in pregnancy . Not safe to use in small people

56
Q

How is fexinidazole given?

A
  1. With food
  2. DOT
57
Q

What are the side effects of suramin?

A

Nephrotoxicity
Allergic reaction

**use with caution in areas of onchocerciasis because kills microfilaria

58
Q

What are the side effects of melarsoprol

A

Arsenic derivative so it can really eff you up.

SJS
Encephalopathy (associated with 50-70% case fatality)
Cardio and renal toxicity

59
Q

What is the prognosis of HAT?

A

Neuro changes can be grossly irreversible or very slow improvement
Death almost certain without treatment

60
Q

When should you follow up your HAT patients?

A

All patients should have follow up LPs for 2 years

Gambiense LP 6 monthly
Rhodesiense LP 3 monthly x 1 year then 6 monthly

61
Q

Why is it difficult to produce a vaccine against HAT?

A

Trypanosomes are coated in Variable Surface Glycoproteins (VSG) each of which has a unique antigen it presents

Basically means it becomes incredibly challenging to create a vaccine because there are hundreds (maybe more) antigenic possibilities in one trypanosome

62
Q

How can HAT be prevented?

A

Tsetse fly traps
Insecticide treated cattle (especially in rhodesiense where cattle act as a reservoir)
Sterilised male tsetses
Case detection and treatment

63
Q

How does Visceral Leishmaniasis present?

A

Low grade Fever
Hepatomegaly
Massive Splenomegaly –> up to the Iliac fossa!!!!
Lymphadenopathy (esp. in Africa for some reason)
Anaemia
Anorexia
Wasting
Increased skin pigmentation

±epistaxis
±cough

64
Q

What are chronic complications of visceral leishmanishs?

A

Anaemia
Manutrition
Wasting
Bleeding
Nephritis
Spelnic Infarcts
Uveitis

65
Q

What is the differential for massive splenomegaly in the tropics?

A

Malaria / hyperreactive malaria splenomegaly
Portal hypertension secondary to schisto
Lymphomas, leukaemias
Splenic hydatid
Amyloidosis

OTHER (moderate):
- Brucellosis
- CMV
- HIV infection
- EBV
- Leptospirosis
- Lyme disease
- Relapsing fever
- Syphilis
- Toxoplasmosis
- Trypanosomisis
- TB
- Typhoid
- Typhus

66
Q

Which three parasites are most assocaited with Visceral Leishmaniasis?

A

Infantum
Chagasi
Donovani

67
Q

Blood tests in Visceral Leish: what might you find?

A

Anaemia
Leucopenia
Thrombocytopenia
Mild ALT/AST/Bili rise
Low Albumin
High Globulins

68
Q

How do you diagnose visceral leish

A

GOLD STANDARD:
identification of amastigotes on microscopy with Giemsa stain
- Splenic aspirates >95% positive
- Bone marrow
- Lymph nodes
- Peripheral Blood (if buffy coat smear)

  1. ELISA
  2. DAT (can remain positive if previous infection)
  3. rK39 rapid antigen test (urinary)
  4. PCR
69
Q

How do you manage Visceral Leishmaniasis?

A

Pentavalent Antimonials (e.g. SSG) + Paromomycin

OR

Liposomal Amphotericin B + Miltefosine

70
Q

What are the side effects of Pentavalent Antimonials?

A

Arthralgia
Nausea
Pancreatitis
Abso pain
Cardiotoxicity

71
Q

What are the side effects of Amp. B?

A

Anaphylaxis
Fever
Chills
Bone pain
Throbophlebitis
Hypokalaemia
Anaemia
Renal impairment

72
Q

What are the side effects of Miltefosine

A

GI upset
Abortifacent and teratogenic
May reduce male fertility

73
Q

How can you prevent Leishmaniasis (5)

A

Early diagnosis and prompt treatment to prevent further cases

Control sandfly populations –> residual sprays, ITNs

Insecticide spraying (DDT)

Health education

Early detection of epidemics

Early diagnosis of HIV co-infection (check all Leish patients for HIV)

Remove reservoir (dog control in SA) or control reservoir (dog collars)

DTM&H (29 decks)

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