Parasitic Infections Flashcards
Define Infection
invasion by and growth of
pathogenic microorganisms
within the body
Define Disease
a disordered or incorrectly functioning organ, part, structure, or system of the body resulting from the effect of genetic or developmental errors, infection, poisons, nutritional deficiency or imbalance, toxicity, or unfavorable environmental factors; illness; sickness; ailment.
Define parasites
Parasite - organism living in or on the host and
dependent on it for nutrition - causing
damage
What is the differences between endoparasites and ectoparasites
Endoparasite – exist INSIDE the host
Ectoparasite – exist on the host (on the skin)
Give some examples of endoparasites
Protozoa: amoeba, coccidiae, ciliate, flagellates
Metazoa: roundworms, flatworms, flukes
What are protozoa
Protozoa – single celled organisms
Eukaryotes (genome within a nucleus, complex organelles in cytoplasm)
Pathogenesis (mechanism of disease) varied
Some have insect vectors (eg malaria)
No eosinophilia
What are metazoan
Metazoa – Multicellular organisms (Helminths/worms)
Free living, intermediate hosts and vectors
Some just inhabit gut (geohelminths), other invade tissues
Eosinophilia – if invade blood
State two amoeba
Amoebae: Entamoeba histolytica, Entamoeba dispar Entamoeba hystolytica (pathogenic)/dispar (commensal)
Entamoeba hystolytica (pathogenic)/dispar (commensal)
Summarise the amoeba organisms
- Entamoeba histolytica
- Entamoeba dispar
Infection occurs by ingestion of mature cysts in food or water, or on hands contaminated by faces- good hygiene is paramount
Describe the epidemiology of amoeba infections
About 10 % of the world’s population is infected with E.histolytica
Third most common cause of death of parasitic infections (after schistomiasis and malaria)
common in South + Central America, West + South-East Asia; rare in temperate climates
~ 90% of infections are asymptomatic; the remaining 10% produce a spectrum of diseases varying from dysentery to amoebic liver abscess
Incubation period may be as short as 7 days; tissue invasion mostly occurs during first 4 months of infection
Outline the life cycle of E.histolytica
Contamination by mature cyst (four nuclei) - by food or water
Excystation- one trophoblastzoite with four nuclei emerges, divides three times and each nucleus divides once to produce 8 trophozoites from each cyst.
Trophozoites migrate to the large intestine and multiply by binary fission
Trophozoites invade the intestinal mucosa – invasive infection through the bloodstream infecting sites such as liver, brain, and lungs
After multiplying by binary fission- one will undergo encystation to form a immature cyst
which then forms a quadrinucleate cyst
cyst will exit in the stool - noninvasive infection
Incubation period may be as short as 7 days; tissue
Describe the key features of the life cycle of E.histolytica
Humans are the only reservoir, and infection occurs by
ingestion of mature cysts in food or water, or on hands
contaminated by faeces.
• The cysts of E. histolytica enter the small intestine and
release active amoebic parasites (trophozoites), which
invade the epithelial cells of the large intestines, causing
flask-shaped ulcers. Infection can then spread from the
intestines to other organs, e.g. liver, lungs and brain, via the
venous system.
• Asymptomatic carriers pass cysts in the feces and the
asymptomatic carriage state can persist indefinitely. Cysts
remain viable for up to 2 months.
Invasive amoebiasis most often causes an amoebic liver
abscess, but may affect the lung, heart, brain, urinary
tract and skin.
E. histolytica (the cause of invasive amoebiasis) must be
differentiated from Entamoeba dispar, which is a normal
commensal of the gastrointestinal tract.
Describe the laboratory diagnosis of amebiasis
E.histolytica and E.dispar are morphologically identical species. In bright-field microscopy, E.histolytica and E.dispar cysts are spherical and usually measure 12-15microns (range may be 10-20 microns). A mature cyst has 4 nuclei, but an immature cyst may only have 1-3 nuclei.
Describe the treatment for amebiasis
Nitroimidazole derivatives (act on trophozoite, but not on cysts) + parmomycine or diloxanide furoate
Summarise the coccidia
Coccidia
Coccidial infection in humans are mostly zoonoses
Plasmodium species - malaria
- Toxoplasma - toxoplasmosis
- Cryptosporidium- diarrhoea
Summarise the different diseases caused by coccidia
Malaria
Toxoplasmosis: mild disease in immunocompetent individuals:
fever, swollen lymph nodes, headaches, sore throat.
however, in pregnancy: toxoplasmosis poses serious danger for the
Foetus)
Diarrhoea (mild disease in immunocompetent individuals,
the parasites can cause serious pathological changes in
immunocompromised individuals)
Describe the different types of plasmodium species
Different types of plasmodium: P. falciparum, P. malariae, P. ovale, P. vivax and P. knowlesi
2 types of host: humans and female Anopheles mosquitoes (~ 20 different Anopheles species are locally important around the world. All of the important vector species bite at night. Anopheles mosquitoes breed in water)
2 stages in human: liver and blood stages
Falciparum more serious
Outline the life cycle for plasmodium
Mosquito takes a blood meal (injects sporozoites) infects liver cell –forming schizont and then a ruptured schizont
Infective- exo-erythrocytic cycle.
Then enters the blood
immature trophozoite (ring stage)
divides to form a mature trophozoite and a gametocyte
mature trophozoite forms a schizont which then ruptures - erythrocytic cycle
gaemtocytes divide by meiosis
mosquito takes a blood meal and ingests gametocytes
forming macro gametocytes with flagellated micro gametocytes
ookinete
oocyst which then ruptures to release sporozoites which will infect another host when the mosquito takes another blood meal.
Describe the epidemiology and symptoms of malaria
In 2013, there were ~198 million cases of malaria, causing an estimated 584 000 deaths, mostly among African children (one child dies every 30 seconds).
Symptoms:
Can appear as early as 7 days but the time between exposure and signs of illness can be as long as one year.
- 9 to 14 days for Plasmodium (P.) falciparum.
- 12 to 18 days for P. vivax and P. ovale.
- 18 to 40 days for P. malariae.
- 11 to 12 days for P. knowlesi.
Fever, headache, chills, vomiting, muscle pain
Paroxysm (cycle in 4-8hrs)
Describe the complications of malaria
Complications of malaria: Severe anemia (destruction of red cells) Cerebral malaria (swelling of the brain,seizures, coma)
liver failure Shock Pulmonary edema abnormally low blood sugar kidney failure swelling and rupturing of the spleen
Describe the treatment of malaria
Uncomplicated malaria:
chloroquine, Atovaquone-proguanil, Artemether-lumefantrine, quinine sulfate plus one of the following: Doxycycline, Tetracycline or Clindamycin Quinine sulfate, Mefloquine
Severe malaria:
Artemisinin-based combination therapy (ACT) is recommended for the treatment of P. falciparum malaria.
Resistance an issue for treatments
Describe the diagnosis of malaria
blood film, Giemsa stained
Rapid test: commercially available antigen detection tests: more expensive and less sensitive
Describe the transmission routes for toxoplasma gondii
Humans can become infected by any of several routes:
• eating undercooked meat of animals harboring tissue cysts
• consuming food or water contaminated with cat feces
• by contaminated environmental samples
• blood transfusion
• organ transplantation
• transplacentally from mother
to fetus.
Infect warm blooded animals
Which group of patients are particularly vulnerable to toxoplasma gondii
Immunocompromised patients may develop central nervous system disease, brain lesions, pneumonitis or retinochoroiditis among other risks.
How do we diagnose toxoplasma gondii
Serological tests are available
What does cryptosporidium cause
Causes diarrhea, fever, nausea, vomiting in humans; very common in HIV+ patients presenting with diarrhea.
cryptosporidiosis
Describe the diagnosis and treatment for cryptosporidiosis
Diagnosis: stool examination.
Treatment: fluid rehydration.
Water is the vector- contaminated oocysts
Summarise ciliates
Balantidium coli
(Balantidiasis)
Reservioir hosts:
Primates
Rodents
Pigs
Worldwide distribution
Summarise balantidiasis
Most people infected with Balantidium coli => no symptoms.
Immunocompromised patients may experience more severe signs and symptoms: persistent diarrhea, dysentery, abdominal pain, weight loss, nausea, and vomiting. If left untreated, perforation of the colon can occur.
Diagnosis: stool examination
Treatable
Summarise flagellates
Giardia lamblia
(Giardiasis)
Giardiasis: commonest, globally distributed, water-borne protozoal
infection.
Flagellated trophozooites attach by their suckers to surface of the
duodenal or jejunal mucosa
Ovoid cysts are able to survive standard chlorination procedures,
filtration is required to exclude them from drinking water
Diarrhoea
Two stages:
trophozoites
cysts
Describe the key features of giardiasis
Epidemiology
~2% of adults and 6% to 8% of children in developed countries worldwide; ~ 33% of people in developing countries
Symptoms Most people infected with Balantidium coli => no symptoms. Acute symptoms: Diarrhea Greasy stools that tend to float Stomach or abdominal cramps Upset stomach or nausea/vomiting Dehydration (loss of fluids)
Diagnosis
Stool examination:
Treatment: metronidazole/tinidazole
How is trichomonas ( a flagellate) transmitted
Transmitted sexually
What is important to remember about trichomoniasis
Trichomoniasis
It is estimated to be the most common, curable, non-viral sexually transmitted infection in the UK, with nearly 6000 new cases per year.
Describe the key features of trichomoniasis
In women the organism is found in the vagina, urethra and paraurethral glands; in men infection is usually of the urethra.
TransmissionIn adults transmission is almost exclusively through sexual intercourse.
Symptoms
Females10-50% are asymptomatic.=> vaginal discharge, vulval itching, dysuria, or offensive odour, but these are not specific for TV.Occasionally the presenting complaint is of low abdominal discomfort or vulval ulceration.
Males
15 to 50% of men are asymptomatic
=> discharge and/or dysuria.
ComplicationsDetrimental outcome on pregnancy and is associated with preterm delivery and low birth weight.
HIV
There is growing evidence that trichomonas infection may enhance HIV transmission and there may be an increased risk of TV infection in those that are HIV positive.
Diagnosis
Microscopy: Detection of motile trichomonads in swab/urine- Trichomonas Rapid Test
Treatment
metronidazole
What is another important flagellate
Flagellates: Leishmania
Summarise the key features of helminths (metazoan)
Complex o Multicellular parasites.
o Cycles may involve insect vectors and intermediate hosts.
For most, humans are the definitive host – a few are zoonoses (acquired from animals).
o Adult worms cannot multiply in man – the number of adults is related to the infection.
o A large burden is found in school-aged children which has a massive effect on their development- massive impact for future economy of the country
Lay eggs, microfilaria, larvae
What are the most common helminth infections worldwide
Ascariasis
Trichuriasis
Hookworm infection
Schistosomiasis
What are the 3 groups of helminths
Roundworms (nematodes) • Ascaria • Hookworms • Filaria • Strongyloides Flatworms (cestodes) • Taenia (tapeworms) Flukes (trematodes) • Schistosoma
Eosinophilia in invasive worms
What can happen upon antihelmnithic treatment in ascariasis
Massive Ascaris infection in a child: a large bolus of roundworms
expelled following antihelminthic treatment
Outline the life cycle of ascaria
Adult worms live in the lumen of the small intestine.
A female may produce up to 240,000 eggs per day,
which are passed with the feces. Fertile eggs
embryonate and become infective after 18 days to
several weeks, depending on the environmental
conditions (optimum: moist, warm, shaded soil).
After infective eggs are swallowed, the larvae
hatch, invade the intestinal mucosa, and are carried
via the portal, then systemic circulation to the lungs.
The larvae mature further in the lungs (10-14 days),
penetrate the alveolar walls, ascend the bronchial
tree to the throat, and are swallowed. Upon
reaching the small intestine, they develop into adult
worms. Between 2 and 3 months are required from
ingestion of the infective eggs to oviposition by the
adult female. Adult worms can live 1 to 2 years.
Describe the pathology of ascariasis
Infection with Ascaris lumbricoides often causes
no symptoms. Infections with a large number of
worms may cause abdominal pain or intestinal
obstruction. Adults feed on the contents of the
small intestine and in heavy infections, this may
compound problems in malnourished
individuals (especially children). Migration of
larvae may cause localized reactions in various
organs. Penetration of the larvae from
capillaries into the lungs can lead to Loeffler’s
pneumonia, in which pools of blood and dead
epithelial cells clog air spaces in the lungs.
Resulting bacterial infections can be fatal.
Describe the diagnosis and treatment of ascariasis
Diagnosis
Stool examination
Treatment
albendazole and mebendazole
Summarise some key features of hookworms (nematodes)
Ancylostoma
duodenale
Iron deficiency
anaemia
Adult hookworms about 1cm long and curved. They are attached by their buccal capsules to the villi of the small intestine
Outline the life cycle of hookworms
Larvae are carried through the blood vessels to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed. The larvae reach the small intestine, where they reside and mature into adults. Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall with resultant blood loss by the host.
Adults can release eggs in the faces- rhabditiform larvae hatches
filariform larva
which can penetrate skin in the ankle in water or face-oral ingestion
Describe the pathology of hookworms
Iron deficiency anemia (caused by blood loss at the site of intestinal attachment of the adult worms) is the most common symptom of hookworm infection, and can be accompanied by cardiac complications. Gastrointestinal and nutritional/metabolic symptoms can also occur. In addition, local skin manifestations (‘ground itch’) can occur during penetration by the filariform (L3) larvae, and respiratory symptoms can be observed during pulmonary migration of the larvae.
Describe the diagnosis and treatment of hookworm
Diagnosis
Stool examination:
Treatment
albendazole and mebendazole
Outline the life cycle for trichuris trichiura (whipworm)
The eggs hatch in the small intestine, and release larvae that mature and establish themselves as adults in the colon. The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location
Unembryonated eggs passed in feces
2-cell stage
advanced cleavege
embryonate eggs are ingested
Describe the pathology of whipworm
Small amounts of whipworms might not cause any symptoms. But if there are hundreds of worms, then you might have bloody diarrhea and anemia due to severe vitamin and iron loss. The worms leave open wounds, which cause inflammation of the intestinal wall. In some cases you might also develop rectal prolapse.
Describe the diagnosis and treatment for whipworm
Diagnosis
Stool examination
Treatment
albendazole and mebendazole
Describe the potential therapeutic uses of whipworm
Whipworm is one of the worms being used in helminthic therapy which helps against allergies and autoimmune diseases
What are the two forms of filaria
Brugia malayi
Wucheria bancrofti
What can filaria cause
Lymphatic filariasis
Elephantiasis
lymphatic obstruction (especially in the legs) can progress to
elephantiasis – can also occur in arm, breast, scrotum
Describe the treatment and diagnosis of filaria
Diagnosis
The microfilariae are found mainly in the peripheral blood and can be found at peak amounts from 10 p.m. to 4 a.m. During the day, they are present in the deep veins, and during the night, they migrate to the peripheral circulation.
Blood smear or antigen detection with a immunochromatic test (card) or ELISA
Treatment: albendazole and ivermectin
Describe the life cycle of filaria
Mosquito takes a blood meal (L3 larvae enter skin)
adults in lymphatics
adults produce sheathed microfilariae that reach the bloodstream
mosquito takes a blood meal (ingests microfilariae)
microfilariae shed sheaths, penetrate the mosquito’s midgut and migrate to thoracic muscles.
L1 larvae
l3 larvae
migrate to had and mosquito’s proboscis
mosquito takes a blood meal (L3 larvae enter skin)
Describe another type of filaria
Loaiasis- Loa loa – Eye worm
Loaiasis: confined to Africa
Adult worm live in man for 4-12 years. Females (~7cm) migrate through the subcutaneous tissues, may cross the front of the eye under the conjunctiva. Microfilariae develop from larvae in the female and circulate in the blood from where they may be picked up by Chrysops and in the gut of the fly, the microfilariae enter the fat bodies and mature into infective third stage larvae. These larvae infect a new host when Chrysops takes a bloodmeal and mature into adult worms within about one year.
Summarise tapeworms
Humans are the only definitive hosts for
T. solium and T. asiatica – pig
T. saginata – beef
Describe the symptoms of Taenia
Most people => no symptoms or mild symptoms. Patients with T. saginata taeniasis often experience more symptoms (size of the worm up to 10m) that those with T. solium or T. asiatica (~3 m). Tapeworms can cause digestive problems including abdominal pain, loss of appetite, weight loss, and upset stomach.
The most visible sign of taeniasis is the active passing of tapeworm segments
Summarise the diagnosis and treatment of Taenia
Diagnosis:
Segment in stool or identifcation of eggs in stool
Treatment:
praziquantel
Describe the life cycle of taenia
Adult tapeworm in small intestine- 8 - 11 foot long
Egg contaminated in vegetation is ingested by livestock
eggs hatch into larvae and infect the animal’s muscles tissue
larvae from cysts in muscle tissue
cysts survive in raw and in raw and undercooked tissue
scolex (head of tapeworm) attaches to intestine
What can taenia solium cause
Taenia solium - cysticercosis
Commonest acquired cause of epilepsy worldwide
Describe the life cycle of schistosomas (trematode)
S. mansoni, haematobium and japonicum
Eggs eliminated in water via feces or urine => hatch and release miricidia => penetrate sail => release as cercariae that will penetrate the skin => will migrate through different tissues and transform into adult male and female worm and will eventually reside in venules. The eggs are moved progressively toward the lumen of the intestine (S. mansoni and S. japonicum) and of the bladder and ureters (S. haematobium).
What are the symptoms of schistomiasis
Within days: possible rash or itchy skin. Within 1-2 months; fever, chills, cough, and muscle aches but most people have no symptoms at this early phase of infection.
When adult worms are present, the eggs that are produced usually travel to the intestine, liver or bladder, causing inflammation or scarring. Children who are repeatedly infected can develop anemia, malnutrition, and learning difficulties. After years of infection, the parasite can also damage the liver, intestine, lungs, and bladder.
Describe the diagnosis and treatment of schistomiasis
Diagnosis:
stool or urine samples
Treatment
praziquantel- can lead to liver damage- liver bleeding
Aklilu Lemma observed that downstream from where people were washing clothes with the soapberry, dead snails were found floating in the water. After several years of intense research, Dr Lemma discovered that the sun-dried and crushed Endod berries were lethal to all major species of snails - but not harmful to animals or humans, and completely biodegradable.
Summarise Sarcoptes scabiei
scabies
Diagnostic
Appearance of rash + presence of burrows- also itchiness
Treatment
Scabicides
Ectoparasites
Adult females deposit eggs as they burrow
egg
egg hatch releasing larvae
larvae malt into nymphs. Larvae and nymphs are found in short burrows called melting patchers
malting occurs after the male penetrates the moulting such of the adult female.
Impregnanted females leave their molting pouches and excavate a permanent burrow in which they lay eggs.
Describe some other ectoparasites
Pediculus humanus capitis (head louse),
Pediculus humanus corporis (body louse, clothes louse), and
Pthirus pubis (“crab” louse, pubic louse)
Three stages: eggs, nymphs (1st,2nd and 3rd) and adult
Transmission by direct contact
Describe the transmission of scabies
Primarily occurs person-to-person, skin-to-skin contact
Occasionally transmission Amy occur via fomites
human scabies mites are often found between the fingers and on the wrists.
Describe the lifecycle of leishmania parasites
Amastigotes in macrophages- ingested by mosquitoes
released from macrophages
multiply
transform (develop flagella)
inoculated into vertebrate host
attachment and phaogocytosis
transform back into amastigotes (lose flagella)
multiplication and reinfection in macrophages- eventually released into blood
Describe the distribution of sandfly
• Sand flies are found mainly in the warm parts of the world,
including southern Europe, Asia, Africa, Australia, Central
and South America
Climate change
In Europe transmission of Leishmania is spreading
Northwards from Greece and Turkey and occurs in
southern France and is currently spreading through
Italy.
Describe the appearance and behaviour of sandflies
They are small and hairy (3mm)
They hop around before settling down to bite
Unlike mosquitoes, they are silent in attack
Female, but not male, feed on blood which
provide nutrition for their eggs.
What are the major forms of leishmaniasis
Visceral Leishmaniasis
Cutaneous Leishmaniasis
Diffuse Cutaneous Leishmaniasis
Mucocutaneous Leishmaniasis
Summarise visceral leishmaniasis
Visceral leishmaniasis (Kala azar): most severe form, fatal if left
untreated. Characterised by irregular fever, weight loss,
swelling of liver and spleen, anaemia
• Also called Kala azar (= black fever)
Describe the key features of visceral leishmaniasis
30-100 subclinical infections
for every overt VL case
Risk factors for development of clinical disease include: • Malnutrition • immune suppressive drugs • HIV co-infections
Describe some symptoms of visceral leishmaniasis
Fever 95% Splenomegaly 95% Uncomfortablespleen 85% Weightloss 80% Anaemia 75% Lymphnodes 75% Lossofappetite 70% Cough 75% Hepatomegaly 60% Oedema 5% Diarrhoea 40% Vomiting 15% Jaundice 5%
What has research on patients shown with visceral leishmaniasis
Reduced BMI
Reduced CD4+ and CD8+ cell counts
Describe the burden of VL
Visceral leishmaniasis (VL) in Ethiopia
Distribution (mapping activity is going on)
involve at least five administrative regions, namely Amhara, Tigray, Southern Nations Nationalities Peoples
Region, Oromia and Somali
Factors associated with spread include:
population movement to and from endemic foci
Annual burden (not determined annual burden ranges from 4,000 – 5,000 cases factors associated with spread include; population movement to and from endemic foci HIV/VL co-infection ranges from 15% to 35%
- Which type of leishmania causes the majority of cases of visceral leishmaniasis in Ethiopia?
L. donovani
vectors- P.martini, p.celiae, p.orientalis
Describe the diagnosis of VL
Clinical diagnosis based on case definition
VL case definition: “a person who presents with fever of more than two weeks and enlarged spleen
(splenomegaly) and/or enlarged lymph node (lymphadenopathy) or either of weight loss, anaemia or
leucopenia while living in a known VL endemic area or having travelled to an endemic area”.
Parasite detection:
definitive diagnosis of VL is made by visualization of the amastigote form of the parasite by
microscopic examination of aspirates from lymph nodes, bone marrow or spleen aspiration
Antibody detection:
Direct agglutination test (DAT) and rK39 chromatographic test
Describe the treatment for VL
First line regimens for primary VL Sodium stibogluconate (SSG) or Meglumin antimoniate (monotherapy) 20 mg/kg/day for 30 days either intramuscular or slow intravenous infusion within 5 minutes
Liposomal Amphotericin B (LAmB, AmBisome®)
VL is 3-5 mg/kg daily or intermittently for 5-7 doses over 6 - 10 days with a total dose of 30 mg/kg
used only in special cases (HIV coinfection, pregnancy and very sick patients)
Combination therapy: Sodium stibogluconate (SSG) and paromomycin- NOT IMPLEMENTED YET
Second line
Liposomal Amphotericin B
Miltefosine (2-3mg/kg per day for 28 days)
- What other clinical manifestation of leishmania can occur during or after treatment for visceral leishmaniasis?
frequent in Sudan and India • in ~55% of patients in Sudan, in 5-10% in India • Occurs during or after treatment, after sub-clinical infection • Lesions start on face, usually around mouth • Lesions can become nodular • PKDL can spread to the trunk and limbs.
Summarise cutaneous leishmaniasis
Cutaneous leishmaniasis: skin lesions on exposed body parts,
often self-healing. Can create serious disability and scars.
Immunity to reinfection
Describe the symptoms of cutaneous leishmaniasis
L. Tropica -crusted ulcer
L. major- multiple crusted lesions
Large, irregular ulcer; surrounded by papular and crusted
lesions which all contain parasites
Summarise diffuse cutaneous leishmaniasis
• Diffuse cutaneous leishmaniasis: disseminated lesions,
resembles leprosy difficult to treat, no spontaneous
healing, frequent relapses
Multiple, nodular non-ulcerating lesions
L. aethiopica: disseminated infection
No spontaeous healing, relapses
Summarise mucocutanous leishmaniasis
Mucocutaneous (L. braziliensis/panamensis)/mucosal (L. infantum, major, tropica, aethiopica)
leishmaniasis: disfiguring, destroys mucous membranes
No spontaeous
healing, relapses
typically effects mouth and nose
Summarise the burden of cutaneous leishmania
Distribution
Mainly in the highlands, between 1,400 - 3,175 meters above sea level: L. aethiopica
Lowland: L. tropica and L. major
Annual burden (not determined) 20,000 to 30,000 cases (rough estimation)
Prevalence of each spectrum (not determined)
Of 354 patients suspected in the laboratory in 2011 (Leishmaniasis Research and Diagnostic Laboratory,
Addis Ababa University)
LCL= 163
MCL=26
DCL= 8
Undefined = 6
Describe the diagnosis of CL
Parasitological diagnosis that involves microscopy and/or culture
- FNA (fine needle aspiration)
- Dermal scraping
- Biopsy
Leishmanin skin test (for epidemiological study)
• Serology
Polymerase chain reaction (PCR)(AHRI)
Describe the treatment of CL
Systemic treatment with Sodium Stibogluconate (SSG) or Glucantime
dosage: 20mg/kg/day (SSG)
- dosage: 20mg/kg/day (Glucantime)
- duration: a minimum of 28 days, usually longer
outcome: very poor prognosis for DCL and MCL
Intra-lesion administration of SSG
Highly variable in terms of dosage and duration
Outcome: variable
Cytotherapy
• Miltefosine (compassionate) Outcome: better prognosis than any of the other options listed specially for DCL but associated with relapse Dosage: 2-3mg/kg per day Duration: minimum of 28 days
Describe the distribution of leishmaniasis
98 countries
~ 2 million new cases/year (1.5 CL, 0.5 VL)
> 350 million people at risk
> 20 Leishmania species
> 30 sandfly species
Describe Leishmania in Europe
Europe: 70% of VL cases are associated with HIV
infection (drug users).
ART: reduced incidence of VL
reduced relapse rates
prolonged the intervals between relapses
improved survival.
Describe Leishmania in Brazil
high parasite load parasite dissemination to unusual sites lower cure rates greater susceptibility to drug toxicity increased drug resistance higher rates of death higher rates of relapse
Describe Leishmania in Ethiopia
Ethiopia carries the greatest burden of HIV-VL co-infection:
high rates of mortality
high rates of relapse
• HIV infection can lead to reactivation of latent Leishmania infection or to symptomatic VL at initial
infection
• 100-1000 x greater risk for HIV+ individuals to develop the disease as compared to HIV- individuals
VL accelerates the onset of AIDS
- increased HIV replication
- cumulative immunosuppression
Describe vectors
o Vector – an organism that transmits a disease or parasite from one organism to another.
Snail – transmits schistosomiasis (Fluke, Metazoa, endoparasite).
Female anopheles’ mosquito – transmits malaria (Coccidia, protozoa, endoparasite).
Chrysops – transmits Loiasis (Roundworm, Metazoa, endoparasite).
Distinguish between ectoparasites and Endoparasites
o Endoparasites – an organism that lives IN a host and is dependent on its function and causes damage to the host.
o Ectoparasites – an organism that lives ON a host and is dependent on its function and causes damage to the host.
What is important to remember about adult worms
Adult worms lay eggs or produce microfilariae but cannot themselves multiply in man- therefore a cause of morbidity rather than mortality.
Summarise the protozoa
These can be divided into:
Amoebae e.g. Entamoeba histolytica can cause a bloody form of diarrhoea (dysentery) when it infects the colon and also can lead to abscess formation in the liver. These amoebae can ingest red cells. Other amoebae e.g. Entamoeba dispar are non pathogenic.
Coccidia- Plasmodium species e.g. P. falciparum, vivax, ovale and malariae (and most recently knowlesi) cause malaria. The life cycle involves the invertebrate (Anopheles mosquito) and vertebrate host (man). In man there is both a liver and a blood component to the cycle.
The major disease forms are a febrile illness, cerebral malaria (alteration in conscious level), respiratory distress and severe anaemia.
– Toxoplasma is another coccidian protozoa which can cause an illness (toxoplasmosis) in the newborn especially involving the retina in the eye, and in immunosuppressed patients (e.g. HIV infected) affecting the brain. Infection is commonly from animals e.g. kitten faeces or undercooked meat.
– Cryptosporidium, another coccidian parasite can infect the small bowel and produces severe diarrhoea. Infection is commonly waterborne. Occurs in the UK.
Flagellates
-Giardia infects the upper small bowel (jejunum) and leads to giardiasis, a troublesome prolonged diarrhoeal illness, sometimes causing malabsorption. The organism has a ventral sucker by which it attaches to the bowel wall and flagellae which provide motility.
– Trypanosoma a flagellated protozoa, transmitted by tsetse flies (often in the vicinity of animals e.g. game parks), lead to a febrile illness with lymphadenopathy and ultimately invades the nervous system leading to alterations in consciousness (sleeping sickness).
– Leishmania are transmitted by sandflies and can lead to a skin or organ (liver, spleen and bone marrow) form of disease (cutaneous and visceral leishmaniasis respectively). Apart from the tropics, the disease also occurs around the Mediterranean and is associated with HIV infection.
– Trichomonas is the commonest protozoal in the UK causing a vaginitis.
Ciliates- Balantidium is an unusual pathogen in man causing diarrhoea.
Summarise the metazoan
Helminths have developed immune evasion mechanisms which allow them to cause chronic illness. Invasive forms lead to eosinophilia (an increase in eosinophil count- one of the granulocytic white blood cells found in the blood).
Round worms (Nematodes) – Ascaris leads to ascariasis in the bowel. Worms can cause obstruction especially of bile duct or if sufficient numbers, the bowel. No intermediate host.
– Filaria can cause a variety of diseases. Lymphatic filariasis (elephantiasis), cutaneous filariasis (onchocerciasis) leading to blindness and loaiasis (eyeworm). Transmitted by Aedes mosquitoes, blackflies and mango flies, respectively.
– Strongyloides is an important worm infestation because the eggs produced by the adults can hatch within the host and invade human tissue leading to severe illness especially when the host is immunocompromised. It is cause of diarrhoeal illness in the tropics. Flat worms (Cestodes) – Taenia infestation (tapeworm) can be from pork (Taenia solium) or beef (Taenia saginata). The importance of the distinction is that the larvae from the eggs of the pig tapeworm can invade the host tissues especially the brain leading to a condition called cysticercosis- with fits and focal neurological signs (e.g. weakness). Flukes (Trematodes) – Schistosoma infection leading to bilharzia is the best example. Infection is acquired by contact with freshwater in which the invasive form (cercaria) penetrate the skin. The adult worms live in either the urinary bladder (S. haematobium) or bowel (S. mansoni) where they lay eggs. The eggs may spread to the liver where they cause an inflammatory reaction leading to fibrosis and obstruction to the portal vein draining the bowel which results in oesophageal varices (dilatation of the veins around the oesophagus) and later haemoptysis (the vomiting of blood).
Summarise the ectoparasites
– Scabies: Sarcoptes scabiei burrow into the upper layer of the skin, causes temporary itching due to dermatitis; do not multiply on the human host.
– Lice: Pediculus humanus capitis, Pediculus humanus corporis, Pthirus pubis; may be asymptomatic or cause tickling feeling, itching, allergic reaction; can serve as vectors for Rickettsia prowazekii (epidemic typhus), Bartonella quintana (trench fever), and Borrelia recurrentis (louse-borne relapsing fever).
Summarise parasites
Conclusion: Parasitic infections are indeed a fascinating and interesting field. They infect much of the world’s population and are an increasing problem in travellers (especially malaria and bilharzia). Where the infectious load is low, clinical presentations may be quite different from those depicted in classical textbooks of medicine. Some have a high mortality e.g. malaria whilst others have high morbidity (e.g. hookworm infection is the commonest cause of an iron deficient anaemia worldwide). These diseases inflict a huge economic burden on those who can afford it least i.e. in developing countries. Sadly they are amongst the greatly neglected diseases of mankind.
