PARASITIC DISEASES.pptx

PARASITIC DISEASES
BY
MBUYE GILBERT YUNKAVI
MLS-FHS-UBa

Introduction
• Man and other living things on earth live in an entangling relationship with each other.
• They don’t exist in an isolated fashion.
• They are interdependent; each forms a strand in the web of life.
• Medical parasitology is the science that deals with organisms living in the human body
(the host) and the medical significance of this host-parasite relationship.
• According to the definition, parasites include the viruses, bacteria, fungi, protozoa and
metazoan (helminths and arthropods).
• Some of these parasites whose existence depends on the availability of hosts are known
as obligate parasites.
• Those which can survive and reproduce without a host are facultative parasites

Introduction
• Very few of these facultative parasites infect humans (e.g. the free-living
amoebae).
• Most of the parasites which live in/on the body of the host do not cause
disease (non-pathogenic parasites).
• In Medical parasitology we will focus on most of the disease causing
(pathogenic) parasites.
• However, understanding parasites which do not ordinarily produce disease
in healthy (immunocompetent) individuals
• but do cause illness in individuals with impaired defense mechanism
(opportunistic parasites) is becoming of paramount importance because of
the prevalence of HIV/AIDS

Some definitions
• Parasite: A parasite is a living organism, which takes its nourishment and other needs from
a host; the host is an organism which supports the parasite
• Different kinds of parasites
• Ectoparasite – a parasitic organism that lives on the outer surface of its host, e.g. lice, ticks,
mites etc.
• Endoparasites – parasites that live inside the body of their host, e.g. Entamoeba histolytica.
• Obligate Parasite - This parasite is completely dependent on the host during a segment or
all of its life cycle, e.g. Plasmodium spp.
• Facultative parasite – an organism that exhibits both parasitic and non-parasitic modes of
living and hence does not absolutely depend on the parasitic way of life, but is capable of
adapting to it if placed on a host. E.g. Naegleria fowleri
• Accidental parasite – when a parasite attacks an unnatural host and survives. E.g.
Hymenolepis diminuta (rat tapeworm).
• Erratic parasite - is one that wanders in to an organ in which it is not usually found. E.g.
Entamoeba histolytica in the liver or lung of humans

Types of hosts
• Definitive host – a host that harbors a parasite in the adult stage or where the
parasite undergoes a sexual method of reproduction.
• Intermediate host - harbors the larval stages of the parasite or an asexual cycle of
development takes place. In some cases, larval development is completed in two
different intermediate hosts, referred to as first and second intermediate hosts.
• Paratenic host – a host that serves as a temporary refuge and vehicle for reaching an
obligatory host, usually the definitive host, i.e. it is not necessary for the completion
of the parasites life cycle.
• Reservoir host – a host that makes the parasite available for the transmission to
another host and is usually not affected by the infection.
• Natural host – a host that is naturally infected with certain species of parasite.
• Accidental host – a host that is under normal circumstances not infected with the
parasite.

Continuation
• There is a dynamic equilibrium which exists in the interaction of organisms.
• Any organism that spends a portion or all of its life cycle intimately associated
with another organism of a different species is considered as Symbiont
(symbiote)
• this relationship is called symbiosis (symbiotic relationships).
• There exist three common symbiotic relationships between two organisms

Types of symbiosis
• Mutualism - an association in which both partners are metabolically dependent upon each
other and one cannot live without the help of the other
• However, none of the partners suffers any harm from the association.
• One classic example is the relationship between certain species of flagellated protozoa
living in the gut of termites.
• The protozoa, which depend entirely on a carbohydrate diet, acquire their nutrients from
termites.
• In return they are capable of synthesizing and secreting cellulases; the cellulose digesting
enzymes, which are utilized by termites in their digestion.
• Commensalism - an association in which the commensal takes the benefit without causing
injury to the host. E.g. Most of the normal floras of the humans’ body can be considered as
commensals.
• Parasitism - an association where one of the partners is harmed and the other lives at the
expense of the other. E.g. Worms like Ascaris lumbricoides reside in the gastrointestinal
tract of man, and feed on important items of intestinal food causing various illnesses

Effect of parasites on the host
• Mechanical injury - may be inflicted by a parasite by means of pressure as it grows larger,
e.g. Hydatid cyst causes blockage of ducts such as blood vessels producing infraction.
• Deleterious effect of toxic substances- in Plasmodium falciparum production of toxic
substances may cause rigors and other symptoms.
• Deprivation of nutrients, fluids and metabolites -parasite may produce disease by
competing with the host for nutrients.
• Indirect effects of the parasite on the host:
• Immunological reaction: Tissue damage may be caused by immunological response of the
host, e.g. nephritic syndrome following Plasmodium infections.
• Excessive proliferation of certain tissues due to invasion by some parasites can also cause
tissue damage in man, e.g. fibrosis of liver after deposition of the ova of Schistosoma.

CLASSIFICATION OF MEDICAL PARASITOLOGY
• Parasites of medical importance come under the kingdom called Protista and
Animalia.
• Protista includes the microscopic single-celled eukaryotes known as protozoa.
• In contrast, helminthes are macroscopic, multicellular worms possessing well
differentiated tissues and complex organs belonging to the kingdom Animalia
• Medical Protozoology - Deals with the study of medically important protozoa.
• Medical Helminthology - Deals with the study of helminthes (worms) that
affect man.
• Medical Entomology - Deals with the study of arthropods which cause or
transmit disease to man

AMOEBIASIS
• Amoebas are primitive unicellular microorganisms with a relatively simple life cycle which
can be divided into two stages:
• Trophozoite – actively motile feeding stage.
• Cyst – quiescent, resistant, infective stage
• The parasite causing amoebic dysentery in humans is Entamoeba histolytica.
• Entamoeba histolytica is found in the human colon.

Epidemiology
• E. histolytica has a worldwide distribution.
• Although it is found in cold areas, the incidence is highest in tropical and subtropical
regions that have poor sanitation and contaminated water.
• About 90% of infections are asymptomatic, and the remaining produces a spectrum of
clinical syndrome.
• Patients infected with E. histolytica pass non-infectious trophozoite and infectious cysts in
their stools.
• Therefore, the main source of water and food contamination is the symptomatic carrier
who passes cysts.
• Symptomatic amoebiasis is usually sporadic.
• The epidemic form is a result of direct person-to-person faecal-oral spread under
conditions of poor personal hygiene.

Pathogenesis and Clinical Features
• Entamoeba histolytica causes intestinal and extra-intestinal amoebiasis.
• The lumen-dwelling amoebae do not cause any illness.
• They cause disease only when trophozoites invade the intestinal tissues.
• The trophozoite penetrates the epithelial cells in the colon, aided by its movement and
histolysin, a tissue lytic enzyme, which damages the mucosal epithelium.
• Amoebic lectin mediates adherence.
• Mucosal penetration produces discrete ulcers with a pinhead center and raised edges.
• Sometimes, the invasion remains superficial and heals spontaneously.
• The ulcers are multiple and are confined to the colon, being most numerous in the caecum
and recto-sigmoidal region.
• The intervening mucous membrane between the ulcers remains healthy, The amoebic ulcer
is flask-shaped in cross-section

• Multiple ulcers may coalesce to form large necrotic lesions with ragged and undermined
edges and are covered with brownish slough.
• The ulcers generally do not extend deeper than submucosal layer.
• Amoebae are seen at the periphery of the lesions and extending into the surrounding
healthy tissues.
• Clinical manifestations are diarrhoea, vague abdominal symptoms and dysentery.
• This may resemble bacillary dysentery, the ulcers may involve the muscular and serous coats
of the colon, causing perforation and peritonitis.
• Blood vessel erosion may cause haemorrhage.
• Deep ulcers form scars and may lead to strictures and partial obstruction.

• A granulomatous pseudotumoral growth may develop on the intestinal wall from a chronic
ulcer.
• This amoebic granuloma or amoeboma may be mistaken for a malignant tumour.
• The incubation period for intestinal amoebiasis varies from 1 to 4 months
• Liver involvement is the most common extra intestinal complication of intestinal
amoebiasis.
• About 5–10% of patients with intestinal amoebiasis will develop amoebic liver abscess
(ALA).
• ALA arises from haematogenous spread of amoebic trophozoites from colonic mucosa or
by direct extension.
• Often, ALA patients do not present with bowel symptoms.
• Liver damage may not be directly caused by the amoebae, but by lysosomal enzymes and
cytokines from the inflammatory cells surrounding the trophozoites.

• The centre of the abscess contains thick brown pus (anchovy sauce), which is liquefied necrotic liver
tissue free of amoeba.
• The trophozoite is in the wall of the abscess. Liver abscess may be multiple or more often solitary,
usually located in the upper right lobe of the liver.
• Jaundice develops only when lesions are multiple or when they press on the biliary tract.
• Large untreated abscess may rupture into the lungs and pericardium.
• The incidence of liver abscess is more common in adult males
• Other complications are;
• Amoebic cerebral abscess
• Amoebic peritonitis
• Genitourinary amoebiasis
• Perianal ulceration
• Pulmonary amoebiasis
• Splenic abscess
• Toxic megacolon

Treatment
• Luminal amoebicides: Diloxanide furoate, iodoquinol, Paromomycin and tetracycline act in
the intestinal lumen but not in tissues.
• Tissue amoebicides: Emetine and chloroquine are effective in systemic infection, but less
effective in the intestine.
• Both luminal and tissue amoebicides: Metronidazole (750–800 mg 3 times daily for 5–10
days), Tinidazole and ornidazole act on both sites
• Carriers should also be treated because of the risk of transmitting the infection to others.
• Paromomycin or iodoquinol should be used in these cases.
• Although metronidazole and tinidazole are both luminal and tissue amoebicides, neither of
them reach adequate levels in the gut lumen.
• Therefore, patients with ALA should also receive treatment with a luminal agent to ensure
eradication of infection.
• Paromomycin (25–35 mg/kg/day, divided into 3 doses for 7 days) is the drug of choice.

Prevention and control
• Boil drinking water
• Wash fruits and vegetables in clean water before eating
• Detection and treatment of carriers and prohibit them from food handling
• Health education

MALARIA
Habitat
• In human, the parasites are found in the erythrocytes and hepatocytes.
Vectors
• Human malaria is transmitted by over 60 species of female Anopheles mosquito.

Plasmodium falciparum (Malignant tertian)
• Plasmodium falciparum demonstrates no selectivity in host erythrocytes, i.e. it invades
young and old RBCs cells.
• The infected red blood cells also do not enlarge and become distorted.
Epidemiology
• P. falciparum occurs almost exclusively in tropical and subtropical regions.
• Weather (rainfall, temperature & humidity) is the most obvious cause of
seasonality in malaria transmission.
• To date, abnormal weather conditions are also important causes of significant
and widespread epidemics.
• Moreover, drug-resistant infection of P. falciparum is the commonest challenge
in many parts of the world

Clinical features
• Of all the four Plasmodia, P. falciparum has the shortest incubation period, which ranges from
7 to 10 days.
• After the early flu-like symptoms, P. falciparum rapidly produces daily (quotidian) chills and
fever as well as severe nausea, vomiting and diarrhoea.
• The periodicity of the attacks then becomes tertian (36 to 48 hours), and fulminating disease
develops. Involvement of the brain (cerebral malaria) is most often seen in P. falciparum
infection.
• Capillary plugging from an adhesion of infected red blood cells with each other and
endothelial linings of capillaries causes hypoxic injury to the brain that can result in coma and
death.
• Kidney damage is also associated with P. falciparum malaria, resulting in an illness called
“black water” fever.
• Intravascular hemolysis with rapid destruction of red blood cells produces a marked
haemoglobinuria and can result in acute renal failure, tubular necrosis, nephrotic syndrome,
and death.
• Liver involvement is characterized by abdominal pain, vomiting of bile,
hepatosplenomegaly, severe diarrhoea, and rapid dehydration.

Treatment
• Because chloroquine – resistant strains of P. falciparum are present in many
parts of the world
• infection of P. falciparum may be treated with other agents including
mefloquine, quinine, guanidine, pyrimethamine – sulfadoxine, and
doxycycline.
• If the laboratory reports a mixed infection involving P. falciparum and P. vivax,
• the treatment must eradicate not only P. falciparum from the erythrocytes
but also the liver stages of P. vivax to avoid relapses provided that the person
no longer lives in a malaria endemic area.

Plasmodium vivax (Benign tertian)
• P. vivax is selective in that it invades only young immature erythrocytes
• Epidemiology
• P. Vivax is the most prevalent of the human plasmodia with the widest geographic
distribution, including the tropics, subtropics, and temperate regions
Clinical features
• After an incubation period (usually 10 to 17 days), the patient experiences vague flu-like
symptoms, such as headache, muscle pains, photophobia, anorexia, nausea and vomiting.
• As the infection progresses, increased numbers of rupturing erythrocytes liberate
merozoites as well as toxic cellular debris and hemoglobin in to circulation.
• In combination, these substances produce the typical pattern chills, fever and malarial rigors.
• These paroxysms usually reappear periodically (generally every 48 hours) as the cycle of
infection, replication, and cell lyses progresses.
• The paroxysms may remain relatively mild or may progress to severe attacks, with hours of
sweating, chills, shaking persistently, high temperatures (1030F to 1060F) and exhaustion.
Since P. vivax infects only the reticulocytes, the parasitemia is usually limited to around 2 to
5% of the available RBCs

Treatment
• Chloroquine is the drug of choice for the suppression and therapeutic
treatment of P. vivax, followed by premaquine for radical cure and elimination
of gametocytes.
Plasmodium malariae (Quartan malaria)
• In contrast with P. vivax and P. ovale, P. malariae can infect only mature
erythrocytes with relatively rigid cell membranes.
• As a result, the parasite’s growth must conform to the size and shape of red
blood cell.
• This requirement produces no red cell enlargement or distortion, but it results
in distinctive shapes of the parasite seen in the host cell, “band and bar forms”
as well as very compact dark staining forms.
Epidemiology
• P. malariae infection occurs primarily in the same sub-tropical and temperate
regions as infections with the other plasmodia but is less prevalent.

Clinical features
• The incubation period for P. malariae is the longest of the plasmodia, usually 18
to 40 days, but possibly several months to years.
• The early symptoms are flu-like with fever patterns of 72 hours (Quartan
malarial) in periodicity
Treatment
• The treatment regimen, including the use of primaquine to prevent relapse
from latent liver stages is similar to that used for P. vivax infection.
Prevention
• Chemoprophylaxis and prompt diagnosis and treatment.
• Control of mosquito breeding
• Protection of insect bite by screening, netting and protective clothing
• Use of insect repellents

Plasmodium ovale
• P. ovale is similar to P. vivax in many respects, including its selectivity for young,
pliable erythrocytes
Epidemiology
• P. ovale is distributed primarily in tropical Africa. It is also found in Asia and
South America
• Clinical features
• The incubation period for P. ovale is 16-18 days but can be longer.
• Clinically, ovale malaria resembles vivax malaria with attacks recurring every
48-50 hours.
• There are however, fewer relapses with P. ovale.
• Less than 2% of RBCs usually become infected.

Treatment
• The treatment regimen, including the use of primaquine to prevent relapse
from latent liver stages is similar to that used for P. vivax infection
Prevention
• Chemoprophylaxis and prompt diagnosis and treatment.
• Control of mosquito breeding
• Protection of insect bite by screening, netting and protective clothing
• Use of insect repellents

Intestinal Worms
Intestinal nematodes
• All nematodes are characterized by their elongated, cylindrical, and unsegmented
bodies.
• The sexes are separate, the males typically being smaller than females.
• More than a million people worldwide are infected with one or more species of
intestinal nematodes.
• These parasites are most common in regions with poor sanitation, particularly in
developing tropical and sub-tropical countries.
• Although nematode infections are not usually fatal, they contribute to malnutrition
and diminished work capacity.
• Because most of the helminthic parasites do not self-replicate, the acquisition of a
heavy burden of adult worms requires repeated exposure to the parasite in its
infective stage (larva or egg) or auto-reinfection must occur

Ascariasis
• Ascariasis is an infection by the nematode Ascaris lumbricoides. It is the most common
helminthic parasite of humans.
Etiology
• Ascariasis is the largest intestinal nematode. The females are between 20 – 35 cm
• in length, while the males vary between 15 and 30cm. The female lays about 200,000 eggs
per day
Epidemiology
• Ascariasis has a worldwide distribution and it is particularly common in regions with poor
sanitation.
• Man may acquire ascariasis by the ingestion of eggs in contaminated foods or rarely drinks.
• More frequently eggs containing embryos reach the mouth directly from the soil via dirty
hands.
• Hence, children are infected more often than adults.

Clinical features
• Most infections are asymptomatic.
• However, in heavier infections abdominal pain or discomfort, nausea,
vomiting, anorexia and passage of adult worms via anus or mouth may occur.
• During the lung phase, about 9 - 12 days after ingestion of the eggs
• The individual may occasionally present with dry cough, chest pain, fever,
wheezing,
• shortness of breath and blood streaked sputum associated with increased
eosinophils in the circulation.
• This condition is called eosinophilic pneumonitis.
• Heavy infestation competes for nutrients and contributes to malnutrition in
children.

Diagnosis
• Depends on the microscopic demonstration of eggs in the stool or recovery of an adult
worm in the stool or after passing through the mouth or nose
Treatment
• Mebendazole
• Adults and children >10 kg = 100 mg po bid for 3 days
• Children < 10 kg = 50 mg po bid for 3 days
• Albendazole
• Adult and children >10 kg = 400 mg po single dose or for 3 days in heavy infections
• Children < 10 kg = 200 mg po single dose or for 3 days in heavy infections
• Pyrantel pamoate 10 mg/kg up to a maximum of 1gm po once
• Piperazine citrate 75mg/kg po once to a maximum of 3.5 gm for adults and children over
12 years; and a maximum of 2.5 gm for children between 2 – 12 years.
• Levamisole 120 – 150 mg po once

Trichuriasis (whip worm infection)
• Trichuriasis is an infection of the human intestinal tract, caused by the nematode Trichuris
trichuira (whipworm).
Epidemiology
• The distribution of Trichuriasis is worldwide, being most abundant in the warm moist
regions of the world.
• The parasite commonly occurs together with Ascaris lumbricoides and likewise mainly
affects children.
• Infection results from the ingestion of eggs in contaminated soil.
• Transmission may occur through the medium of food or water or directly from the hands of
individuals.
• Children may be heavily infected and constitute important reservoirs.

The life cycle of Trichuris trichuira

Clinical features
• Trichuriasis is asymptomatic in most persons.
• However, children tend to acquire heavier infection and some may experience anorexia,
nausea and abdominal pain.
• Occasionally it causes bloody or mucoid diarrhea in young infants.
• Heavy and chronic infections may cause rectal prolapse.
• Moderately heavy whip worm burdens also contribute to growth retardation
Diagnosis
• Depends on microscopic detection of the characteristic lemon shaped egg of the parasite in
the stool

Treatment
Mebendazole
• Adults and children >10 kg = 100 mg po bid for 3days
• Children < 10 kg = 50 mg po bid for 3 days
Albendazole
• Adults and children >10 kg = 400 mg po daily for 3 days
• Children <10 kg = 200 mg po daily for 3 days

Hook Worm Infection
• Hookworm infection is caused by one of the two hookworm species; namely Ancylostoma
duodenale and Necator americanus.
• Adult hookworms, which are about 1cm long, use buccal teeth or cutting plates to attach to
the small bowel mucosa and ingest blood and intestinal fluid (0.2 ml /day per Ancylostoma
adult)
• This causes large volume blood loss from intestinal bleeding.
• One-fourth of the world's population is infected with one of the two hookworm species.
• Hookworm disease develops from a combination of factors such as heavy worm burden,
prolonged duration of infection, and an inadequate iron intake
• it is characterized by iron deficiency anemia and occasionally hypoproteinemia.

Epidemiology
• Hookworm infection is wide spread and is one of the most important helminthic infections of
man.
• It occurs in nearly all subtropical and tropical countries.
• The distribution of the two species overlap and both are present in many regions of the
world
• In most areas, older children have the greatest incidence and intensity of hookworm
infection.
• In rural areas where fields are fertilized with night soil, older working adults may also be
heavily infected.

The life cycle of hook worm
N.B. The period from skin penetration to appearance of eggs
in the feces is about 4- 6 weeks

Clinical Features
• Most hookworm infections are asymptomatic.
• However, infective larvae may provoke itching rash at the site of skin penetration.
• Moreover, larvae migrating through the lungs occasionally cause mild transient pneumonitis
in the early intestinal phase.
• Infected persons may develop epigastric pain, diarrhea and other abdominal symptoms.
• However, the major consequence of chronic hookworm infection is blood loss resulting in
iron deficiency
• which in marginally nourished individuals may manifest with anemia and hypoproteinemia

Diagnosis
• Microscopic recovery of the typical eggs
• Concentration techniques may be required to detect light infections
Treatment
• Mebendazole, albendazole or Pyrantel pamoate: similar to ascariasis
• Dietary therapy: supplementation of oral iron preparations for iron deficiency
anemia, plus proteins & vitamins.

Enterobiasis
• Enterobiasis is an infection of the human intestinal tract by Enterobius vermicularis (the
pinworm)
Etiology and Life Cycle
• Enterobius vermicularis is a spindle shaped parasite of man and attaches to the mucosa of
the lower ileum, caecum and ascending colon.
• Pinworm eggs are infective shortly after being excreted.
• After ingestion, the eggs hatch in the upper intestine and liberate larvae which migrate to
the region of the ileum.
• Copulation (mating) of the worms takes place in the lower small intestine
• The females migrate to the caecum or lower bowel and pass through the anus where upon
contact with the air they shower their sticky eggs on the perianal skin.

Epidemiology
• Enterobiasis is a worldwide disease infecting mostly children Infections occur by ingestion of
the eggs that reach the mouth on soiled hands or in contaminated food or drink.
• The intense perianal itching is an important factor in autoinfection and maintenance of the
primary reservoir.
• Because of the predominance of person-to-person transmission, autoinfection through the
perianal-fecal-oral route and through egg contamination of blankets and clothing,
• Enterobiasis is more common in some families and institutions
• (orphanages, boarding schools, asylums, and refugee camps) where people live under
crowded conditions

Clinical features
• Most pinworm infections are asymptomatic.
• The most common symptom when present is intense perianal itching.
• It is worse at night and may lead to excoriation and bacterial superinfection.
• Heavy infections may manifest with abdominal pain, anorexia and weight loss.
Diagnosis
• Eggs are not typically found in the stool because they are released on the perineum.
• Therefore, eggs deposited in the perianal region are detected from perianal swab or
• by the application of clear cellulose tape to the perianal region in the morning.
• The tape is then transferred to slide to be seen under a microscope

Treatment
• 1 . Drugs of choice:
• Mebendazole
• Adult and children >1 0 kg = 1 00 mg po once then repeat same dose in 2 weeks
• Children < 1 0 kg = 50 mg po once then repeat same dose in 2 weeks OR
• Albendazole
• Adult and children >1 0 kg = 400 mg po single dose then repeat same dose in 2
• weeks
• Children < 1 0 kg = 200 mg po single dose then repeat same dose in 2 weeks
• 2. Alternatives:
• Pyrantel pamoate 1 1 mg/kg po maximum 1 .0 gram single dose then repeat same dose in
2 weeks
• Warm tap water enema may help
• Family members should be treated to decrease potential source of reinfection

Strongyloidiasis
• Strongyloidiasis is an infection by the nematode Strongyloides stercoralis.
• It is usually embedded in the mucosa and sub mucosa of the small intestine of
man.
• The adult parasite is small in size, the female measuring about 2.2mm in length.
• The mature female lies buried in the mucosa and sub mucosa of the intestine where it
liberates eggs.
• The eggs hatch to produce the rhabditiform larvae that are passed in the stool.
• The rhabditiform larvae may undergo further development in either of two ways:

• As free living adult under suitable conditions of moisture and temperature or
• As infective filariform larvae under unfavorable conditions
• These infective larvae are capable of penetrating the skin of man.
• After skin penetration the filariform larvae reach the lymphatics or capillaries and are
carried to the right side of the heart and pulmonary capillaries.
• Here they leave the capillary beds and penetrate into the alveoli of the lungs.
• Then most of them migrate up the respiratory passages, reach the esophagus and pass
down into the stomach and intestines.
• The larvae mature to adult female worms in the small intestine and penetrate its mucosa.
• Finally mature female worms produce eggs that hatch and maintain continuity of the cycle.
• Besides skin penetration by infective larvae, autoinfection is commonly observed in this
disease

• The autoinfection cycle involves the change of rhabditiform larvae to filariform larvae within
the bowel lumen
• Their penetration either the perianal skin or the wall of the intestine maintain the cycle in
the absence of reinfection.
Epidemiology
• Strongyloides stercoralis is patchily distributed in tropical areas particularly in Sub-Saharan
Africa and South East Asia.
• Human beings usually acquire the infection by skin penetration of the infective filariform
larvae
• Due to its “autoinfective” life cycle, Strongyloidiasis can become permanently established in
humans without the need to reinfection and a chronic clinical syndrome occurs
• In such cases there is a potential for “Hyperinfection syndrome” where host immunity is
reduced
• This is due to steroid or immunosuppressive drug therapy, severe malnutrition, leukemia and
lymphoma, DKA, post irradiation treatment and lepromatous leprosy

Clinical Features
• A) Uncomplicated Strongyloidiasis
• Many patients are asymptomatic or have mild cutaneous and /or abdominal
symptoms.
• Cutaneous manifestations include recurrent urticaria involving the buttocks
and wrists, and an itchy skin lesion along the courses of larval migration.
• Abdominal symptoms include epigastric pain which resembles peptic ulcer
disease, nausea, diarrhea, and mild intestinal bleeding.
• The migration of larvae through the lungs may cause cough & occasionally
severe respiratory symptoms.
• In HIV patients the clinical courses are protracted, but the complication is
uncommon for unknown reasons.

Clinical Features
• B) Disseminated Strongyloidiasis (hyperinfection syndrome)
• In this case, the larva may invade not only the intestinal and lung tissues, but
also the central nervous system, liver, and kidneys.
• Patients may have severe and often bloody diarrhea, bowel inflammation with
multiple micro-perforations,
• Bacterial peritonitis and paralytic ileus, gram-negative sepsis,
• Hemoptysis, pleural effusion and hypoxia, encephalitis, and bacterial
meningitis.

Diagnosis
• In uncomplicated Strongyloidiasis, the finding of rhabditiform larvae in feces is
diagnostic.
• Single stool examination detects only about one third of infections.
• Therefore, serial stool examination or use of concentration techniques should
be employed to improve the sensitivity of stool diagnosis.
• In hyperinfection syndrome, on the other hand, the larvae are easy to find in
the stool or other body fluids
• (pleural, peritoneal, or bronchoalveolar lavage samples).

Treatment
• Even in the asymptomatic state, strongyloidiasis must be treated because of its potential for
fatal hyper infection.
• Asymptomatic or uncomplicated cases:
• Drug of choice: Ivermectin 200µg/kg/d po (or 6 mg po/d) for 3 days
• Alternatives:
• Thiabendazole 25mg/kg bid maximum of 3 gm/d for two days OR
• Albendazole 1 5 mg/kg twice a day maximum of 400 mg daily for three days repeat same
dose after 7 days.
• Complicated cases (hyperinfection syndrome):
• Drug of choice: Ivermectin 200µg/kg/d po (or 6 mg po/d) for 3 days
• Alternatives:
• Thiabendazole for five to seven days or albendazole for two weeks.
• Supportive therapy: it is also important to manage complications such as gram negative
sepsis, pneumonia or meningitis

Prevention and control of intestinal nematodes
• Health education
• Sanitary disposal of feces in latrines and avoid use of night soil as fertilizer
• Improve personal and food hygiene practices
• Improve standard of living conditions
• Concurrent disinfections of human excreta
• Investigation of contact and source of infection
• Treatment of the infected cases

Diphyllobothrium latum (Fish tapeworm/Broad tapeworm)
• Distribution
• Its infection occurs in central and northern Europe, particularly in the Scandinavian
countries.
• It is also found in Siberia, Japan, North America and Central Africa.
• Dogs, cats and many wild animals may be naturally infected.
• Habitat
• The adult worm is found in the small intestine of human, usually in the ileum

• Infection may be asymptomatic, while some patients may present with intestinal
obstruction.
• Abdominal discomfort, diarrhoea, nausea, weakness, weight loss and
• anaemia are the usual manifestations.
• The worm lives in the ileum where vitamin
• B12 absorption takes place.
• It competes with the host for vitamin B12 and may cause
• vitamin B12 deficiency anaemia.
Diphyllobothrium latum. (a) Scolex, (b) Gravid proglottids, (c)
Egg

• Diagnosis
1. Microscopic examination
Detection of operculated eggs or gravid proglottids in faeces.
• The arrangement of the uterus in gravid proglottid at its center is frequently likened
to a rosette.
2. Molecular diagnosis
PCR on clinical specimens.
Treatment
Praziquantel (5–10 mg/kg orally in a single-dose therapy). Parenteral vitamin B 12
should be given in vitamin B12deficiency anaemia.
Prevention and Control
1. Proper cooking of fih
2. Deep freezing of fih (–10 °C for 24–48 h)
3. Proper sanitation
4. Periodical deworming of pet dogs and cats as they can be infected by eating
contaminated raw fih
5. Treatment of cases

Taenia saginata and Taenia solium (Beef tapeworm and Pork tapeworm respectively)
• Taenia saginata and Taenia solium have a worldwide distribution
• Habitat
• The adult worms of both T. saginata and T. solium live in the small intestine of human
Taenia solium. (a) Scolex, (b) Gravid proglottid, (c) Larvae
(cysticercus cellulosae)
Egg of Taenia

• Intestinal taeniasis can be caused by both T. saginata and T. solium.
• It is mostly asymptomatic.
• In symptomatic infection, patient presents with vague abdominal discomfort,
indigestion, nausea, diarrhoea and weight loss.
• Cases of acute intestinal obstruction and acute appendicitis have been reported.
• Cysticercosis is caused by larval stage (cysticercus cellulosae) of T. solium.
• Humans acquire infection after ingesting eggs of T. solium in contaminated food or
water.
• Any organ or tissue may be involved, the most common being subcutaneous tissues,
brain and eye.
• The cysticercus is surrounded by a fibrous capsule except in the eye and ventricles of
the brain.
• The degenerating larvae evoke a cellular reaction with infiltration of neutrophils,
eosinophils, lymphocytes and plasma cells.
• This is followed by fibrosis and death of the larva which eventually calcify

• The clinical features depend on the site affected.
• Subcutaneous nodules are mostly asymptomatic.
• Muscular cysticercosis may cause acute myositis.
• Neurocysticercosis (cysticercosis of the brain) is the most common and serious form of cysticercosis.
• The majority of adult onset epilepsy is due to neurocysticercosis.
• Headache is also a common manifestation of neurocysticercosis.
• In ocular cysticercosis, patients may present with blurred vision or loss of vision
• Diagnosis of Taeniasis
• 1. Microscopic examination
• Detection of characteristic eggs, scolex, or gravid proglottids of Taenia in feces.
• Species identification cannot be made from the eggs since the eggs of T. saginata and T. solium look alike.
• Eggs can also be detected around the perianal region by the cellophane swab technique.
• 2. Molecular diagnosis
• PCR on fecal samples.

• Diagnosis of Cysticercosis
• 1. Serodiagnosis
• 2. Biopsy
• HPE examination of biopsied lesion to show the invaginated scolex with suckers and hooks.
• 3. Imaging
• Calcified cysticerci can be detected by radiography of subcutaneous tissue and muscles.
• X-ray of the skull may demonstrate calcified cyst in the brain.
• CT scan of brain is the best method for detecting dead calcified cysts.
• MRI scan of the brain is more helpful in detection of non-calcified cysts and ventricular cysts.
• Treatment
• 1. Intestinal taeniasis
• Praziquantel (5–10 mg/kg orally in a single-dose therapy) is the drug of choice.
• Niclosamide (2 g orally in a single-dose therapy) is an alternative drug.

• 2. Cysticercosis
• Excision is the best method, where the cysts are accessible.
• For cerebral cysticercosis, Praziquantel (50 mg/kg in 3 divided doses daily for 15 days) and
albendazole (15 mg/kg daily (maximum 800 mg/day) for 8 days) may be administered.
• Corticosteroids may be given along with Praziquantel or albendazole to reduce the inflammatory
reactions caused by the dead cysticerci.
• Antiepileptic drugs should be given.
• Surgical intervention is indicated for hydrocephalus.
• Prevention and control
1. Proper cooking of beef and pork
2. Proper sanitation
3. Personal hygiene
4. Avoid eating raw vegetables grown in polluted soil to prevent from acquiring
cysticercosis
5. Treatment of cases with taeniasis solium as they can develop cysticercosis due to
autoinfection

Echinococcus granulosus (Dog tapeworm)
• Distribution
• The hydatid disease caused by E. granulosus is prevalent in most parts of the world
• It is most extensive in the sheep and cattle rearing countries (Australia, Africa and South
America).
• Habitat
• The adult worm lives in the small intestine of dogs and other canine.
• The larval stage (hydatid cyst) is found in humans and herbivorous animals (sheep, goat,
cattle and horse).

• Hydatid cyst infection is often asymptomatic.
• Clinical illness develops when the hydatid cyst causes obstruction or pressure effect.
• In majority of cases, the primary hydatid cyst occurs in liver, mostly in the right lobe.
• Clinical manifestations are hepatomegaly, pain and obstructive jaundice.
• The next common site is the lower lobe of the right lung.
• Cough, haemoptysis, chest pain, pneumothorax and dyspnoea are the usual presentation.
• In the kidney, hydatid cyst causes pain and haematuria.
• Other sites affected include spleen, brain, pelvic organs, orbit and bones.
• Cerebral hydatid cysts may present as focal epilepsy.
• Hydatid cyst in bones may cause pathological fractures.
• Hypersensitivity to hydatid fluid seeping through the capsule may cause urticaria.
• Massive release of hydatid fluid from spontaneous rupture or surgical procedure may cause
anaphylactic shock.

• Diagnosis
• PCR on clinical specimens.
• Detection of scolices and hooklets from aspirated cyst fluid.
• 4. Imaging
• Radiological examinations and other imaging techniques such as ultrasonography (USG), CT scan and MRI.
• Treatment
• Puncture, aspiration, injection and reaspiration (PAIR) is carried out in early stages of the disease.
• Surgical treatment in cases where the cysts are accessible.
• Patients with small or multiple cysts can be treated with albendazole (400 mg twice/day for 1–6 months).
• Praziquantel may be useful prior to surgery or in cases of spillage of cyst contents during surgery
• Prevention and Control
• 1. Prevent dogs from eating animal carcass or offal
• 2. Periodical deworming of dogs
• 3. Personal hygiene

Hymenolepis nana (Dwarf tapeworm)
• Distribution
• It is cosmopolitan in distribution but is more common in tropical countries
• Infection is most common in children.
• Habitat
• The adult worm lives in the ileum of human

• Hymenolepiasis is usually asymptomatic but in heavy infections, patients may present with nausea,
anorexia, abdominal pain, diarrhoea and irritability.
• Anal pruritus may be due to an allergic response.
• Diagnosis
• Detection of characteristic eggs in faeces.
• Treatment
• Praziquantel (25 mg/kg in a single-dose therapy) is the drug of choice.
• It acts both against the adult worms and the cysticercoids in the intestinal villi.
• Alternative drug is nitazoxanide.
• 1. Personal hygiene
• 2. Proper sanitation
• 3. Avoid consumption of contaminated food and water by fla or beetles
• 4. Rodent control

Schistosomiasis
• Schistosomiasis is a trematode disease caused by different species of Schistosoma
• Trematodes are parasites that commonly infect the human intestine, biliary tree, lung, and
venules of the genitourinary tract or intestine.
• Trematodes can be
• Tissue (organ) dwelling trematodes include species like Fasciola hepatica and
• Fasciolopsis buski infects the lung, intestine, and biliary tree
• Blood-dwelling trematodes include Schistosoma species that reside in venules
• Trematodes have three morphologic stages
• 1 ) The egg (ova) – the excretory stage
• 2) Larvae (Miracidium, metacercariae, cercariae)- the infective stage
• 3) Adult worms.

Etiology
• Four species of Schistosoma namely;
• Schistosoma mansoni,
• S. japonicum,
• S. makongi
• S. intercalatum are responsible for intestinal schistosomiasis
• S. haematobium for urinary schistosomiasis

Pathogenesis
• Infection occurs during body contact with water contaminated with infective cercariae.
• The duration and intensity of infection, host genetics, concurrent infection, and location of
egg deposition govern the disease manifestations.
• Allergic reaction to the schistosomula or eggs is responsible for the acute manifestations,
• while inflammatory and fibrotic responses to eggs are responsible for chronic
manifestations.
• -Tissue reaction to retained eggs, which follows sensitization to egg antigens, is a circumoral
granuloma.
• It results from a combined humeral and cell-mediated attack on the egg, and it is
characteristically composed of epitheloid, giant cells,
• Lymphocytes and eosinophils are arranged in a concentric circle around the egg.
• The cellular components of granuloma diminish with time or disappear following
chemotherapy

Epidemiology
• There are a number of reservoir hosts capable of carrying schistosoma species, especially in
the case of s. Japonicum.
• Snails are intermediate hosts in which the asexual stage (larval stage) develops.
• Snails are more likely found in stagnant than rapidly flowing water.
• The snail species are specific to each Schistosoma species
• i.e. Biomphalaria for S mansoni, Onchomelania for S. japonicum and Bulinus for
• S.hematobium.
• S.mansoni is scattered in Africa, S. America, the Caribbean and parts of Arabia.
• S.mansoni and S.hematobium are the species endemic in Ethiopia

Clinical manifestation
• Patients with schistosomiasis may have different clinical features based on host
• factors, site of infection (intestinal, urinary) parasite load and duration of
infection.
• The manifestations occur in 4 stages
• Stage one (stage of invasion): Patients may have itching sensation at the site of
• skin penetration by cercariae (called swimmers’ itch).
• It occurs in travelers to endemic areas and is rare in indigenous people
• Stage two (acute schistosomiasis): Patients may have diarrhea, abdominal
cramp, tenesmus, fever and chills. .

• Stage three and four (Chronic or hepatosplenic schistosomiasis):
• Patients with S. mansoni may present with complications like periportal
fibrosis with portal hypertension
• (causing abdominal swelling (ascites), splenomegaly, and upper GI
• bleeding from varices) intestinal stricture and polyps.
• Chronic manifestations of S.hematobium include obstructive uropathy from
fleshy masses in the bladder
• (pseudopapillomas) with the resulting hydroureter & hydronephrosis
occasionally followed by uremia.
• Moreover, S.hematobium is known to cause bladder calcification, genital
involvement (urethral papillomatosis of men and boys
• and sterility of women) and cor-pulmonale

Diagnosis
• - It is essential to have a high index of suspicion for patients coming from
endemic areas.
• - Confirmation of the diagnosis is by detection of ova using direct microscopic
examination of;
• stool or rectal biopsy specimen in the case of S. mansoni
• Urine sediment in S. haematobium.
• The egg of S.mansoni is characterized by lateral spine, while that of
S.hematobium by a terminal spine.

Treatment
• Praziquantel is the drug of choice for both S mansoni and S.hematobium.
• Additionally, Oxaminoquine is effective against S mansoni and Metrifonate is
• effective for S.hematobium.
• All these drugs are safe and effective.
• Doses are given below:
• S mansoni
• Praziquantel – 40 mg/kg as a singe dose or in two divided doses given 4 hours apart
• Oxaminoquine 1 5 mg/kg bid for two days
• S.hematobium
• Praziquantel – same dose as above
• Metrifonate – 22.5 – 30 mg/kg divided into 3 doses and given weekly for 3 weeks

Leishmaniasis
Clinical disease
• Visceral leishmaniasis (Kala azar or Black fever)
• Cutaneous leishmaniasis
• Mucocutaneous leishmaniasis
• The species of leishmania exist in two forms, amastigote (aflagellar) and
promastigote (flagellated) in their life cycle.
• They are transmitted by certain species of sand flies (Phlebotomus &
Lutzomyia)

Visceral leishmaniasis (kala-azar (“black sickness”) or dumdum
fever
• Etiologic agent; Leishmania donovani
Important features
• The natural habitat of L. donovani in man is the reticuloendothelial system of
the viscera
• The amastigote multiplies by simple binary fission until the host cells are
destroyed, whereupon new macrophages are parasitized.
• In the digestive tract of appropriate insects, the developmental cycle is also
simple by longitudinal fission of promastigote forms.
• The amastigote stage appears as an ovoidal or rounded body, measuring about
• 2-3μm in length
• The promastigotes are 15-25μm lengths by 1.5-3.5μm breadths

Pathogenesis
• In visceral leishmaniasis, the organs of the reticuloendothelial system (liver,
• spleen and bone marrow) are the most severely affected organs.
• Reduced bone marrow activity, coupled with cellular destruction in the spleen,
results in anaemia, leukopenia and thrombocytopenia.
• This leads to secondary infections and a tendency to bleed.
• The spleen and liver become markedly enlarged, and hypersplenism
contributes to the development of anaemia and lymphadenopathy also
occurs.
• Increased production of globulin results in hyperglobulinemia, and reversal of
the albumin-to-globulin ratio

Epidemiology
• L. donovani , infection of the classic kala-azar (“black sickness”) or dumdum
fever type occurs in many parts of Asia, Africa and Southeast Asia.
• Kala-azar occurs in three distinct epidemiologic patterns.
• In Mediterranean basin (European, Near Eastern, and Africa) and parts of
China and Russia, the reservoir hosts are primarily dogs & foxes
• In sub-Saharan Africa, rats & small carnivores are believed to be the main
reservoirs.
• In India and neighboring countries (and Kenya), kala-azar is anthroponosis, i.e.
there is no other mammalian reservoir host other than human.

Epidemiology
• The vector is the Phlebotomus sand fly.
• Other variants of L. donovani are also recognized: L. donovani infantum with
similar geographical distribution, reservoir host and vector; with L. donovani
donovani.
• L. donovani chagasi is found in South America, Central America, especially
Mexico, and the West Indies.
• Reservoir hosts are dogs, foxes, and cats, and the vector is the Lutzomyia sand
fly.

Clinical features
• Symptoms begin with intermittent fever, weakness, and diarrhea; chills and
• sweating that may resemble malaria symptoms are also common early in the
infection.
• As organisms proliferate & invade cells of the liver and spleen, marked
• enlargement of the organs, weight loss, anemia, and emaciation occurs.
• With persistence of the disease, deeply pigmented, granulomatous lesion of
skin, referred to as post-kala-azar dermal leishmaniasis, occurs.
• Untreated visceral leishmaniasis is nearly always fatal as a result of secondary
infection.
Immunity
• Host cellular and humoral defense mechanisms are stimulated

Laboratory diagnosis
• Examination of tissue biopsy, spleen aspiration, bone marrow aspiration or lymph node
aspiration in properly stained smear (e.g. Giemsa stain).
• The amastigotes appear as intracellular & extra cellular L. donovani (LD) bodies.
• Culture of blood, bone marrow, and other tissue often demonstrates the promastigote stage
of the organisms.
• Serologic testing is also available
Treatment
• The drug of choice is sodium stibogluconate, a pentavalent antimonial compound.
• Alternative approaches include the addition of allopurinol and the use of pentamidine or
amphotericin B.
Prevention
• Prompt treatment of human infections and control of reservoir hosts.
• Protection from sand flies by screening and insect repellents

Old World Cutaneous Leishmaniasis (Oriental sore)
• Clinical disease
L. tropica minor - dry or urban cutaneous leishmaniasis
L. tropica major - wet or rural cutaneous leishmaniasis
L. aethiopica - cutaneous leishmaniasis
• Important features
• These are parasites of the skin found in endothelial cells of the capillaries of the
• infected site, nearby lymph nodes, within large mononuclear cells, in neutrophilic
• leukocytes, and free in the serum exuding from the ulcerative site.
• Metastasis to other site or invasion of the viscera is rare.

Pathogenesis
• In neutrophilic leukocytes, phagocytosis is usually successful
• In macrophages the introduced parasites round up to form amastigote and
multiply.
• In the early stage, the lesion is characterized by the proliferation of
macrophages that contain numerous amastigotes.
• There is a variable infiltration of lymphocytes and plasma cell.
• The overlying epithelium shows acanthosis and hyperkeratosis,
• which is usually followed by necrosis and ulceration

Epidemiology
• Cutaneous leishmaniasis produced by L. tropica complex is present in many
parts of Asia, Africa, Mediterranean Europe and the southern region of the
former Soviet Union.
• The urban Cutaneous leishmaniasis is thought to be an anthroponosis while the
rural cutaneous leishmaniasis is zoonosis with human infections occurring only
sporadically.
• The reservoir hosts in L. major are rodents. L. aethiopica is endemic in Ethiopia
and Kenya.
• The disease is a zoonosis with rock & tree hyraxes serving as reservoir hosts.
• The vector for the old world cutaneous leishmaniasis is the Phlebotomus sand
fly

Clinical features
• The first sign, a red papule, appears at the site of the fly’s bite.
• This lesion becomes irritated, with intense itching, and begins to enlarge &
ulcerate.
• Gradually the ulcer becomes hard and crusted and exudes a thin, serous
material.
• At this stage, secondary bacterial infection may complicate the disease.
• In the case of the Ethiopian cutaneous leishmaniasis, there are similar
developments of lesions,
• They may also give rise to diffuse cutaneous leishmaniasis (DCL) in patients
who produce little or no cell mediated immunity against the parasite.
• This leads to the formation of disfiguring nodules over the surface of the body

Immunity, treatment and prevention
• Immunity
• Both humoral and cell mediated immunity (CMI) are involved
• Treatment
• The drug of choice is sodium stibogluconate, with an alternative treatment of
applying heat directly to the lesion.
• Treatment of L. aethiopica remains to be a problem as there is no safe and
effective drug.
• Prevention
• Prompt treatment & eradication of ulcers
• Control of sand flies & reservoir hosts.

New World Cutaneous and Mucocutaneous Leishmaniasis
(American cutaneous leishmaniasis)
• Clinical disease:
• Leishmania mexicana complex- Cutaneous leishmaniasis.
• Leishmania braziliensis complex- mucocutaneous or cutaneous leishmaniasis
• Important features:
• The American cutaneous leishmaniasis is the same as oriental sore.
• But some of the strains tend to invade the mucous membranes of the mouth, nose, pharynx,
and larynx either initially by direct extension or by metastasis.
• The metastasis is usually via lymphatic channels but occasionally may be the bloodstream

Pathogenesis
• The lesions are confined to the skin in cutaneous leishmaniasis and to the
mucous membranes, cartilage, and skin in mucocutaneous leishmaniasis.
• A granulomatous response occurs, and a necrotic ulcer forms at the bite site.
• The lesions tend to become superinfected with bacteria.
• Secondary lesions occur on the skin as well as in mucous membranes.
• Nasal, oral, and pharyngeal lesions may be polypoid initially, and then erode to
form ulcers
• The ulcers expand to destroy the soft tissue and cartilage around the face and
larynx.
• Regional lymphadenopathy is common.

Epidemiology
• Most of the cutaneous & mucocutaneous leishmaniasis of the new world exist in enzootic
cycles of infection
• It involves wild animals, especially forest rodents.
• Leishmania mexicana occurs in south & Central America, especially in the Amazon basin, with
sloths, rodents, monkeys, and raccoons as reservoir hosts.
• The mucocutaneous leishmaniasis is seen from the Yucatan peninsula into Central &
• South America, especially in rain forests where workers are exposed to sand fly bites while
invading the habitat of the forest rodents.
• There are many jungle reservoir hosts, and domesticated dogs serve as reservoirs as well.
• The vector is the Lutzomyia sand fly

• Clinical features
• The types of lesions are more varied than those of oriental sore and include Chiclero ulcer,
Uta, Espundia, and Disseminated Cutaneous Leishmaniasis.
• Laboratory diagnosis
• Demonstration of the amastigotes in properly stained smears from touch preparations of
ulcer biopsy specimen.
• Serological tests based on fluorescent antibody tests.
• Leishman skin test in some species.
• Immunity
• The humoral and cellular immune systems are involved
• Treatment
• The drug of choice is sodium stibogluconate.
• Prevention
• Avoiding endemic areas especially during times when local vectors are most active.
• Prompt treatment of infected individuals

TRYPANOSOMIASIS
• Etiologic agents
• Trypanosoma brucei complex – African trypanosomiasis (sleeping sickness)
• Trypanosoma cruzi – American trypanosomiasis (Chagas’ disease)
• Important features
• These species may have amastigote, promastigote, epimastigote, and trypomastigote stages
in their life cycle.
• In human trypanosomes of the African form, however, the amastigote and promastigote
stages of development are absent.
• Typical trypanosome structure is an elongated spindle-shaped body that more or less tapers
at both ends, a centrally situated nucleus,
• A kinetoplast posterior to nucleus, an undulating membrane arising from the kinetoplast and
• proceeding forward along the margin of the cell membrane and a single free flagellum at the
anterior end.

African trypanosomiasis
• Trypanosoma gambiense & Trypanosoma rhodesiene are causative agents of
the African trypanosomiasis,
• Transmitted by insect bites.
• The vector for both is the tsetse fly

Pathogenesis
• The trypomastigotes spread from the skin through the blood to the lymph node
and the brain.
• The typical somnolence (sleeping sickness) usually progresses to coma as a result
of demyelinating encephalitis.
• In acute form, cyclical fever spike (approximately every 2 weeks) occurs that is
related to antigenic variation.
• As antibody mediated agglutination and lysis of the trypomastigotes occurs, the
fever subsides.
• With a few remains of antigenic variants new fever spike occurs and the cycle
repeats itself over a long period

Epidemiology
• T. burcei gambiense is limited to tropical west and central Africa, correlating with the range
of the tsetse fly vector.
• The tsetse flies transmitting T. b. gambiense prefer shaded stream banks for reproduction
and proximity to human dwellings.
• People who work in such areas are at greatest risk of infection.
• An animal reservoir has not been proved for this infection.
• T. burcei rhodesiense is found primarily in East Africa, especially the cattle-raising
countries, where tsetse flies breed in the brush rather than along stream banks.
• T.b. rhodeseines also differs from T.b. gambiense in that domestic animal hosts
• (cattle and sheep) and wild game animals act as reservoir hosts.
• This transmission and vector cycle makes the organism more difficult to control than T.b.
gambiense.

Clinical features
• Although both species cause sleeping sickness, the progress of the disease is different.
• T. gambiense induced disease runs a low-grade chronic course over a few years.
• One of the earliest signs of disease is an occasional ulcer at the site of the fly bite.
• As reproduction of organisms continues, the lymph nodes are invaded, and fever, myalgia,
arthralgia, and lymph node enlargement results.
• Swelling of the posterior cervical lymph nodes is characteristic of Gambian sleeping sickness
and is called winterbottom’s sign.
• Chronic disease progresses to CNS involvement with lethargy, tremors, meningoencephalitis,
mental retardation, and general deterioration
• In the final stages, convulsions, hemiplegia, and incontinence occur
• The patient becomes difficult to arouse or obtain a response from, eventually progressing to
a comatose state.

Clinical features
• Death is the result of CNS damage and other infections, such as pneumonia.
• In T. rhodesiense, the disease caused is a more acute, rapidly progressive disease that is
usually fatal.
• This more virulent organism also develops in greater numbers in the blood.
• Lymphadenopathy is uncommon, and early in the infection, CNS invasion occurs, resulting in
lethargy, anorexia, and mental disturbance.
• The chronic stages described for T. gambiense are not often seen, because in addition
• to rapid CNS disease, the organism produces kidney damage & myocarditis, leading to death

Immunity
• Both the humoral and cellular immunity involve in these infections.
• The immune responses of the host to the presence of these parasites, however, is faced
with
• antigenic variation, in which organisms that have changed their antigenic identity
• can escape the host immune response and initiate another disease process with
• increased level of parasitemia.

Treatment and prevention
• Treatment
• The same treatment protocol is applied for these parasites.
• For the acute stages of the disease the drug of choice is suramin with
pentamidine as an alternative.
• In chronic disease with CNS involvement, the drug of choice is melarsoprol.
• Alternatives include trypars amide combined with suramin.
• Prevention
• Control of breeding sites of tsetse flies and use of insecticides.
• Treatment of human cases to reduce transmission to flies.
• Avoiding insect bite by wearing protective clothing & use of screen, bed netting
and insect repellants

American trypanosomiasis (Chagas disease)
• Trypanosoma cruzi is a pleomorphic trypanosome that includes an additional form of
amastigote in its life cycle.
• The vector for transmission are reduviid bugs
Pathogenesis
• During the acute phase, the organism occurs in blood as a typical trypomastigote and in the
reticuloendothelial cells as a typical amastigote.
• The amastigotes can kill cells and cause inflammation, consisting mainly of mononuclear
cells.
• Cardiac muscle is the most frequently and severely affected tissue.
• In addition, neuronal damage leads to cardiac arrhythmias and loss of tone in the colon
(megacolon) and esophagus (megaesophagus).
• In the chronic phase, the organism persists in the amastigote form.

Epidemiology
• T. cruzi occurs widely in both reduviid bugs and a broad spectrum of reservoir animals in
North, Central, and South America.
• Human disease is found most often among children in South and Central America, where
there is direct correlation
• between infected wild animal reservoir hosts and the presence of infected bugs whose nests
are found in human dwellings
Clinical features
• Chagas’ disease may be asymptomatic acute or chronic disease.
• One of the earliest signs is development at the site of the bug bite of an
erythematous and indurated area called a chagoma.
• This is often followed by a rash and edema around the eyes and face; in young
children frequently an acute process with CNS involvement may occur.

Clinical features
• Acute infection is also characterized by fever, chills, malaise, myalgia, and
fatigue.
• The chronic Chagas’ disease is characterized by hepatosplenomegaly,
myocarditis
• There is also enlargement of the esophagus and colon
• as a result of the destruction of nerve cells (E.g. Auerbach’s plexus) and other
• tissues that control the growth of these organs.
• Involvement of the CNS may produce granulomas in the brain with cyst
formation and a meningoencephalitis.
• Death from chronic Chagas’ disease results from tissue destruction in the many
• areas invaded by the organisms, and sudden death results from complete heart
block and brain damage.

Immunity
• Unlike African trypanosomiasis, the antigenic variation is less common in T.
cruzi infection.
• Therefore, the humoral and cellular immune responses function in the immune
system.
Treatment
• The drug of choice is nifurtimox.
• Alternative agents include allopurinol & benzimidazole.
Prevention
• Bug control, eradication of nests
• Treating infected person & exclusion of donors by screening blood.
• Development of vaccine

DRACONTIASIS
• Also known as dracunculiasis
• Cased by the nematode Dracunculus medinensis (also known as Guinea worm, Medina
worm, serpent worm, or dragon worm)
• Dracontiasis is characterized by nodular dermatosis produced by the development of
parasite in the subcutaneous tissue.
• Habitat:
• Adult females inhabit the subcutaneous tissue usually of the foot or lower limbs.
• Less frequently they also inhabit other parts of the body including the head and neck.
• Mode of transmission
• Water containing infected Cyclops is the main source of infection.
• Man acquires infections by drinking water contaminated with Cyclops harboring third-stage
larvae.

Pathogenesis:
• The third-stage larva is not pathogenic and does not produce any pathological
lesions.
• Only female adult worm is pathogenic.
• It produces a toxin, forming a blister which is formed at the site at which the
female worm comes out of the surface of the skin on coming into contact with
water.
• The blister is filled with fluid that is bacteriologically sterile and contains
numerous larvae and leucocytes.
• Diffusible toxins produced by the parasite are believed to cause urticaria,
dyspnea, vomiting, mild fever, and occasional fainting.

• The pre-patent period is 10-14 months.
• The symptoms are manifested during parturition of the female and are due to the liberation
of a toxic substance causing allergic manifestation and blister formation.
• Septic infection can occur as a result of contamination by secondary organisms drawn in by
the worm at the time of retraction.
• Blister formation appears wherever the female worms make an attempt to come to the
surface of the body where they can readily discharge their larva.
• The blister is usually found on the lower extremities of the body, especially between the
metatarsal bones, sole of the feet, or on the ankle, and less frequently in arms, buttocks,
scrotum, head, neck, and female breasts.
• Blister formation is accompanied by intense burning pain, a ‘fiery serpent’.
• This may be accompanied by generalized reactions such as urticaria, nausea, vomiting,
diarrhea, and giddiness, and marked burning sensation over the next few days the lesions
vesiculates and blister ruptures producing a painful ulcer.

• The worm is often visible in the opening of the ulcer.
• If the female worms break during the attempts of extraction the larva remains
trapped in the subcutaneous tissue and may give rise to cellulitis and
abscesses.
• In uncomplicated cases, lesions may only last for several weeks until the worm
is completely expelled.
• However, many cases of infection of the worm tracks with the persistence of
the lesions, chronic ulceration, and possible sequelae,
• This involves disseminated infection, phlegma of limbs, contractures of
tendons, fibrous ankylosis or arthritis in the joints, die premature and
calcification.
• The calcified worms can trigger arthritis, locked joints, or permanent clipping
and deformations.

Laboratory diagnosis:
• Detection of adult worms:
• This is possible when the female worm appears at the surface of the skin.
• Detection of first-stage larva:
• Specific diagnosis is made by the microscopic demonstration of the first-stage larva in the
discharge fluid.
• Intradermal test:
• Infection of Dracunculus antigens intradermally causes a wheal to appear in the course of 24
hours in positive cases.
• X-ray examination:
• Worms in deeper tissue after death either become calcified or absorbed.
• The position of the calcified worm may be located by skiagraphy.
• Blood examination
• Serodiagnosis:
• IFA, IHA, ELISA, and western blot are the frequently used test for the demonstration of
circulating antibodies in the serum for the diagnosis of dracunculiasis.

Treatment
• There is no specific drugs or medicines to treat or prevent the disease.
• The mainstay of treatment is the extractions of the adult worm from the patient using a stick
at the surface and wrapping the worm or few cm per day.
• Full extraction can take several days or weeks.
• Topical antibodies are applied to prevent secondary bacterial infections and the affected
body part is bandaged with fresh gauze to protect the site.
• Surgical removal of worm using local anesthesia is another method of treatment
• Albendazole, Mebendazole, Niridazole, thiabendazole and metronidazole are used as anti-
inflammatory agents.
• Analgesics such as aspirin or ibuprofen are given to help reduce the pain and inflammation.

Prevention and control
• The disease can be transmitted only by drinking contaminated water and can be completely
prevented through relatively simple measures.
• Preventing people from drinking Cyclops-contaminated water:
• Avoid drinking contaminated water
• Filtering water
• Boiling
• Treatment of water with larvicides to kill Cyclops
• Preventing people infected with the worm from entering water sources used for drinking.
• Epidemiology
• D. medinensis infection is reported from 18 century of the world.
• The infection is particularly widespread in Africa and the middle east.
• About 140 million people are estimated to suffer from dracunculiasis

FILARIASIS
• A parasitic disease caused by the nematode worms of the Filaria spp.
• These worms burrow through the skin, creating blisters that eventually discharge pus
• The filarial worms reside in the subcutaneous tissues, lymphatic system, or serous cavities
of humans.
• The female worms are ovoviviparous and release larvae known as microfilariae
• The microfilariae can be detected in the peripheral blood or cutaneous tissues, depending
on the species.
• Presence of microfilariae in peripheral blood can exhibit nocturnal periodicity, diurnal
periodicity or no periodicity at all
• The basis of periodicity is unknown but it may be an adaptation to the biting habits of the
vector

Filarial Worms
• The life cycle of filarial nematodes is completed in 2 hosts:
• definitive host (human) and intermediate host (blood-sucking arthropods).
• The microfilariae complete their development in the arthropod host to produce the
infective larval stage.
• Adult worms have a lifespan of many years in the human body whereas microfilariae survive
for a few months

Filarial Worms Causing Lymphatic Filariasis
Wuchereria bancrofti
• Distribution
• Wuchereria bancrofti is distributed widely in the tropics and subtropics
• Habitat
• The adult worms reside in the lymphatic system of human.
• The microfilariae are found in blood.
• The vector or intermediate host of W. bancrofti is Culex quinquefasciatus
Wuchereria bancrofti microfilaria

• The pathogenesis of W. bancrofti infection is dependent on the immune system and
inflammatory responses of the host.
• Infection may present as asymptomatic, inflammatory (in acute phase) and obstructive (in
chronic phase)
• Asymptomatic phase may consist of high microfilaraemia.
• In the endemic regions, patients may show no overt symptoms of lymphatic filariasis.
• In the inflammatory (acute) phase, the antigens from the adult worms elicit inflammatory
responses.
• It is characterized by high fever, lymphatic inflammation (lymphangitis and lymphadenitis)
and lymphoedema.
• These symptoms subside after 5–7 days.
• Other symptoms that may occur include orchitis and epididymitis.
• The obstructive (chronic) phase is caused by blockage of lymph vessel and lymph nodes by
the adult worms

• The affected lymph nodes and vessels are infiltrated with macrophages, eosinophils,
lymphocytes and plasma cells.
• The vessel walls become thickened and the lumen narrowed, causing lymph stasis and
lymph vessel dilatation.
• It may cause granuloma formation, with subsequent scarring and even calcification.
• Inflammatory changes damage the valves in lymph vessels, further aggravating lymph stasis.
• Increased permeability of lymph vessel walls lead to leakage of protein-rich lymph into the
tissues.
• This produces the typical hard pitting or brawny oedema of filariasis.
• Fibroblasts invade the oedematous tissues, laying down fibrous tissue, producing the non-
pitting gross oedema of elephantiasis.
• Chronic lymphatic filariasis is also characterized by lymph varices, lymph scrotum, hydrocele
and chyluria (lymph in urine).
• Involvement of the genitalia and chyluria are characteristics of W. bancrofti infection and not
of B. malayi infection.

• Microfilariae are not normally present in the chronic phase.
• Elephantiasis affects men mainly in the legs, arms and scrotum.
• In women, the legs, arms and breasts are affected.
• Elephantiasis in B. malayi infection involves the leg below the knee.
• Incubation period is about 8–12 months.
• Adult filarial worm contains endosymbiotic bacteria, Wolbachia spp. which has a role in the
pathogenesis of its infection and is also essential for worm fertility.
• It has become a target for antifilarial chemotherapy.
• In tropical pulmonary eosinophilia (TPE), there is a failure in the suppression of immune
response to microfiariae antigens so that microfiariae are filtered out and destroyed in the
lungs with allergic inflammatory reaction.
• TPE is a hypersensitivity reaction to filarial antigen.
• Patient may present with low-grade fever, loss of weight and pulmonary symptoms such as
dry nocturnal cough, dyspnoea and wheezing.

• Children and young adults are more commonly affected in endemic areas.
• There is persistent eosinophilia.
• Chest X-ray shows changes similar to miliary tuberculosis.
• It is associated with a high level of serum IgE and filarial antibodies.
• Serological tests are usually strongly positive.
• Microfiariae are absent in peripheral blood.
• The condition responds to treatment with diethylcarbamazine (DEC), which acts on
microfiariae.
• This condition may be caused by W. bancrofti, B. malayi, or by some animal filarial species.

Diagnosis
• Detection of microfiariae in thick blood film, chylous urine and hydrocele fluid stained with
Giemsa.
• It is best to collect ‘night blood’ samples between 10 pm and 2 am.
• When the microfiariae density is low, concentration techniques such as Knott’s concentration
technique and nucleopore filtration can be used.
• DEC provocation test is useful to bring out the microfiariae into peripheral circulation for
blood collection during day time.
• Immunochromatographic test (ICT)
• Blood samples can be collected at any time of the day.
• PCR on clinical samples

• Treatment
• Diethylcarbamazine (DEC) (6 mg/kg/day orally either 1 day or 12 days.
• One day treatment is generally as effective as the 12-day regimen) is the drug of choice.
• Ivermectin (400 μg/kg single dose orally) can also be used.
• Tetracyclines have an effect in the treatment of filariasis by inhibiting endosymbiotic
bacteria (Wolbachia species).
• In elephantiasis, it requires elevation of the affected limb, use of elastic bandage and foot
care to reduce symptoms.
• Surgery is required for hydrocele.
• Medical management of chyluria includes bed rest, high protein diet and treatment with
DEC.
• 1. Control of the vector mosquito (anti-larval, anti-adult)
• 2. Using mosquito net and mosquito repellants
• 3. Detection and treatment of cases

Brugia malayi
• Distribution
• Brugia malayi occurs in India, Indonesia, Philippines, Malaysia, Thailand, Vietnam, China,
South Korea and Japan.
• Besides B. malayi, another species of this genus includes Brugia timori which is found in
Timor, Indonesia.
• Habitat
• The adult worms reside in the lymphatic system of human.
• The microfiariae are found in blood
Brugia malayi microfiariae

Brugia malayi
• The life cycle of B. malayi is similar to that of W. bancrofti.
• However, the intermediate host of Brugia are vectors of genera Mansonia, Anopheles and
Aedes.
• Pathogenesis, clinical features, laboratory diagnosis and treatment are similar to W. bancrofti
• B. malayi shows nocturnal periodic (microfiariae are not detectable in the blood for the
majority of the day, but the microfilarial density peaks between 10 pm and 2 am)
• Nocturnal sub periodic forms (microfiariae are present in the blood at all times, but appear
at greatest density between noon and 8 pm).
• The nocturnal periodic form is transmitted by Mansonia and some Anopheline mosquitoes in
open swamps and rice growing areas.
• Natural animal infections are rare.
• The nocturnal subperiodic form is transmitted by Mansonia in forest swamps.
• Natural zoonotic infections are common

Filarial Worms Causing Subcutaneous Filariasis
• Loa loa (Eye worm)
• Geographical Distribution:
• The Distribution of L. loa is restricted to the equatorial rain forest area of west and central
Africa.
• Habitat:
• Adults: In connective tissues under the skin, in the mesentery and the parietal peritoneum.
• They commonly migrate rapidly in the body and may be seen in the subconjunctival tissue
of the eye or in thin skinned areas.
• Microfilariae: In peripheral blood of man during day time.
• Infective larvae: In the gut, mouth parts and muscles of tabanide flies of the genus
Chrysops.
• The microfilaria appear in peripheral circulation only during the day from 12 noon to 2 pm
(diurnal periodicity).

• The adult migration through subcutaneous tissues causes temporary inflammation,
• which appear as swellings, of up to 3 cm in size, usually seen on the extremities.
• These are the calabar swellings or fugitive swellings.
• Swellings disappear in a few days, only to reappear elsewhere.
• Ocular manifestations occur when the worm reaches the subconjunctival tissues during its
migration.
• Laboratory Diagnosis
• 1. Finding the characteristic microfilariae in stained blood films taken during the day time.
• 2. Occasionally the microfilariae can be found in joint fluid

• Treatment
• DEC (8–10 mg/kg orally in 3 divided doses daily for 21 days) is effective against both the adult
and the microfiarial forms of L. loa.
• Severe adverse reactions may develop following the sudden death of large numbers of
microfiariae after giving DEC
• Administration of corticosteroids at the same time minimizes such reaction.
• Surgical removal of the migrating adult worms that are found in the conjunctiva or under the
skin.
• 1. Avoiding areas where Chrysops are found
• 2. Avoid vector bites by using insect repellents and protective clothing
• 3. Treatment of positive cases

Onchocerca volvulus
• Causes Onchocerciasis (River Blindness)
• Distribution
• Mainly in tropical Africa, Central and South America.
• A small focus of infection exists in Yemen and south Arabia.
• Habitat
• The adult worms are in nodules in subcutaneous connective tissue of infected persons
• Day biting female black fly of the genus Simulium is the intermediate host.
• The vector Simulium species breed in fast-flowing rivers, hence, the disease is most
• common along the course of rivers and it is also known as ‘river blindness’.
• The adult worm lives in the human host for about 15 years and the microfiariae for about 1
year.
• Humans are the only definitive host.

• Pathogenesis depends on the host’s allergic and inflammatory reactions to the adult worms
and microfiariae.
• The subcutaneous nodule or onchocercoma containing adult worms is a circumscribed, firm,
non-tender and it is formed as a result of fibroblastic reaction around the worms.
• Nodules measure from a few mm to about 10 cm.
• They tend to occur over anatomical sites where the bones are superficial, such as the scalp,
scapulae, ribs, elbows, iliac crest, sacrum and knees.
• Microfiariae cause lesions in the skin and eyes
• The skin lesion is a dermatitis with pruritus, pigmentation, atrophy and fibrosis.
• Ocular manifestations range from photophobia to gradual blurring of vision, progressing to
blindness.
• Lesions may develop in all parts of the eye.
• The most common early finding is conjunctivitis with photophobia.
• Other ocular lesions include punctate or sclerozing keratitis, iridocyclitis, secondary
glaucoma, chorioretinitis and optic atrophy

• Diagnosis
• Detection of microfiariae from skin snip.
• The specimen is best collected around midday.
• 2. Biopsy
• In patients with ocular manifestations, microfiariae may be found in
conjunctival biopsies.
• Adult worms can be detected in the biopsy material of the subcutaneous
nodule.
• PCR of skin snips.

• Treatment
• Ivermectin (150 mg/kg once) is the main stay of treatment. DEC and suramin
have also been used.
• A 6-week course of doxycycline is given to target Wolbachia.
• Surgical excision is recommended when nodules are located on the head due to
the proximity of the worm to the eyes.
• 1. Vector control (larvicides)
• 2. Insect repellents and protective clothing
• 3. Treatment of patients

Trichomoniasis
• Causative agent; Trichomonas vaginalis, a urogenital flagellate
• In human, it lives mainly in the vagina and cervix of females.
• In males, it occurs mainly in the anterior urethra
• It is distributed worldwide.
• Trophozoites live in the vagina and cervix and may also be found in Bartholin’s
• glands, urethra and urinary bladder in females.
• In males, it occurs mainly in the anterior urethra, but may also be found in the
prostate.
• Trophozoites multiply by longitudinal binary fission
• Trophozoites in vagina or orifice of urethra can be found in the vaginal and
prostatic secretions and urine

Trichomoniasis
• Life cycle of T. vaginalis is completed in a human host.
• There is no cystic stage.
• The trophozoite is transmitted directly from person to person.
• Sexual transmission is the usual mode of infection
• Trichomoniasis often coexists with other sexually transmitted diseases; like
candidiasis, gonorrhoea, syphilis, or human immunodeficiency

• Trichomonas vaginalis infects the vagina and secretes cysteine, proteases, lactic
acid and acetic acid
• which disrupt the glycogen levels and lower the pH of the vaginal fluid.
• Trophozoite does not invade the vaginal mucosa.
• The infection can range from mild irritation to severe inflammation
• Infection is often asymptomatic, particularly in males, although some may
develop urethritis, epididymitis and prostatitis
• In females, it may produce severe itching in the genital area with foul smelling
• yellowish green frothy discharge, dysuria, burning sensation with urination and
dyspareunia.
• Cervical erosion is common.
• The incubation period is 4 days to 4 weeks.

• Treatment
• Treatment of both sexual partners is recommended.
• Metronidazole is the drug of choice (250 mg 3 times daily for 10 days).
• In pregnancy, metronidazole is safe to be given in second and third trimesters.
• 1. Treatment of sexual partner
• 2. Patients should be advised to abstain from sexual intercourse until they and
their partners have completed treatment and follow-up

Toxoplasmosis
• Caused by the coccidian Toxoplasma gondii
• Toxoplasma gondii is cosmopolitan in distribution, with the widest range of
hosts
• ranging from birds and warm-blooded animals including humans
• In human, the parasites are found in the tissue, commonly in the
musculoskeletal, brain and eye.
• the parasite occurs in 3 forms:
• 1. Oocyst
• 2. Tachyzoite
• 3. Tissue cyst
• All 3 forms occur in cat which is the definitive host

Toxoplasmosis
• Modes of transmission to human are by eating uncooked or undercooked
infected meat containing tissue cysts,
• ingestion of infective oocysts (through food, water or fingers contaminated
with oocysts),
• intrauterine infection from mother to foetus (congenital toxoplasmosis)
• Blood transfusion or organ transplantation from infected donors.
Toxoplasma gondii. (a) Zoites, (b) Tissue cyst

• Toxoplasma gondii is an opportunistic parasite.
• Most human infections are asymptomatic.
• Clinical toxoplasmosis may be congenital or acquired and the manifestations depend on the
immune status of the infected person.
• Toxoplasmosis may cause fatal complications in AIDS patients.
• Congenital toxoplasmosis occurs when T. gondii is transmitted transplacentally from mother
with primary Toxoplasma infection to foetus.
• The risk of foetal infection increases with the progress of pregnancy and severity of foetal
damage is highest when infection is transmitted in the fist trimester of pregnancy.
• Most infected newborns are asymptomatic at birth and may remain so throughout.
• Some develop clinical manifestations of toxoplasmosis weeks, months and even years after
birth.
• The manifestations of congenital toxoplasmosis include chorioretinitis, intracerebral
calcifications, psychomotor disturbances and hydrocephalus.

• Acquired toxoplasmosis is mostly asymptomatic.
• The most common manifestations of acute acquired toxoplasmosis are cervical
lymphadenopathy, fever, headache, myalgia and splenomegaly.
• The illness may resemble viral infection and is self-limiting.
• Rarely but some may present with pneumonitis, myocarditis and
meningoencephalitis which can be fatal.
• Toxoplasmosis in immunocompromised patients may be due to reactivation of
chronic or latent infection.
• Involvement of the brain is most common, causing toxoplasmic encephalitis.
Symptoms may include headache, confusion, ataxia, hemiparesis and seizures.

Treatment
• Only symptomatic cases are treated.
• Combination drugs of choice are pyrimethamine (25–50 mg daily for 1 month)
and sulfadiazine (2–6 g daily for 1 month) with folinic acid to prevent bone
marrow suppression.
• Pyrimethamine is teratogenic.
• Pregnant mother in fist trimester can be given spiramycin in replacement of
pyrimethamine.
• For congenital toxoplasmosis, daily oral pyrimethamine and sulfadiazine with
folinic acid are given for 1 year
• Systemic corticosteroid may be added to reduce chorioretinitis.
• Patients with ocular toxoplasmosis are treated for 1 month with
pyrimethamine plus either sulfadiazine or clindamycin.

Treatment
• AIDS patients who are seropositive for T. gondii and have a CD4+ T lymphocyte
count below <100/ μL, should receive primary prophylaxis against toxoplasmic
encephalitis.
• Trimethoprim-sulfamethoxazole (Bactrim) (160mg trimethoprim; 800 mg
sulfamethoxazole orally once daily) is the drug of choice.
• If trimethoprim-sulfamethoxazole cannot be tolerated by patients,
dapsonepyrimethamine is the recommended alternative drug of choice.
• Prophylaxis against toxoplasmic encephalitis should be discontinued in patients
who have responded to anti-retroviral therapy (ART) and whose CD4+ T
lymphocyte count is above 200/ μL for 3 months.

Prevention and Control
• Individuals at risk, particularly pregnant women, children and
immunocompromised persons should avoid contact with cat and its faeces
• Proper cooking of meat
• Proper washing of hands, washing of vegetables and fruits before eating
• Screening for T. gondii antibody on all blood donors
• Pet cats should be fed with canned or cooked food
• Cats’ faeces should be discarded daily
• Currently, there is no effective vaccine available for humans

Scabies
• Scabies is a common communicable skin infestation caused by a mite.
• This mite, Sarcoptes scabiei, is sometimes known as the human itch or mange
mite
• due to the intense itching caused when the pregnant female mite burrows into
the top layer of skin and lays eggs
• The term scabies is believed to be derived from the Latin term scabere, which
means to
• scratch, or possibly from the term scabs, which are secondary to bacterial
infection
• It is estimated that more than 300 million cases of scabies occur worldwide
every year
• Anyone who has had contact with the mite can catch scabies

• Scabies spreads rapidly under crowded conditions where there is frequent skin-
to-skin contact between people
• such as hospitals, institutions, child-care facilities, and nursing homes.
• In young, healthy persons scabies is generally considered to be more of a
nuisance than a disease.
• In elderly persons, or those who are immunocompromised, scabies is generally
not diagnosed until cutaneous (skin) lesions and symptoms are apparent.
• Because of the long incubation period, many people can be exposed to scabies
before the infested person is diagnosed

• Sarcoptes scabiei infestation is specific to humans and is different from the
mite infestations that affect dogs and other animals,
• which are more commonly known as mange.
• Mites from mange-infested animals can burrow into human skin but cannot
reproduce, so they die within a few days
• Male mites live only 1-2 days and spend this time seeking out unmated
females.
• Most eggs are removed from the skin by bathing, scratching, or rubbing of the
skin
• Once away from the human body, mites do not survive more than 48-72 hours.

Habits and Habitat
• The most frequent S. scabiei burrow sites are in the folds of skin around the
wrists and in the webbing between the fingers
• Other common sites are the elbows, feet, and ankles; axillae; buttocks; genital
regions; and for women, breasts
• The location of burrows in infants and young children differs somewhat from
that of adults
• commonly involving the palms, sides, soles of the feet, and the head and neck
region.
• Rashes may also occur on other parts of the body and are often caused by the
burrowing of immature stages and unfertilized female mites.
• Unlike adults, children often develop rashes on the face, chest and back.
• Feeding activity and host immune system response to mite secretions and fecal
matter are the sources of irritation
• that lead to scratching, scabbing, and subsequent secondary infections.

• The severity of scabies infestation is directly related to the number of mites residing on the
skin and the length of time between initial infestation and subsequent diagnosis and
treatment.
• Fewer than 10-15 mites may be present on an infested person who is otherwise healthy.
• If diagnosis and treatment are delayed, the number of live mites multiplies resulting in
heavier or atypical infestations.
• Keratotic or crusted scabies, sometimes referred to as Norwegian scabies, was first
• described in persons diagnosed with leprosy in Norway
• This severe form of scabies occurs when treatment for infestation has been delayed for
many months or when a person is immunocompromised, and is characterized by thick,
crusted lesions.
• Imbedded within these crusts are thousands to millions of live mites
• There are several physiological and immunological factors that influence the progression of
infestation

• Persons diagnosed with renal failure, insulin dependent diabetes, or severe
mental retardation may progress from typical to atypical scabies
• in a shorter period of time than healthy persons.
• Crusted scabies is more commonly associated with persons diagnosed with
acquired immunodeficiency syndrome (AIDS),
• T cell leukemia and those who are receiving steroids or immunosuppressive
therapy

Pathogenesis and clinical features
• When a person is infested with scabies mites for the first time, there is usually
little
• evidence of infestation for the first month (range 2 to 6 weeks)
• After this time, and in subsequent infestations, people can become sensitized
to mites and noticeable symptoms generally occur within 1 to 4 days
• The earliest and most common symptom of scabies is intense itching over most
of the body, especially at night.
• This itching can occur in areas where mites are undetectable.
• The accompanying itching usually leads to scratching and excoriation of the
affected areas, contributing to an eczema-like condition
• Secondary bacterial infection can occur due to the excoriation of the skin.

Pathogenesis and clinical features
• Another obvious sign of scabies infestation is a rash of the skin that can appear
as red
• bumps, burrows (short, wavy thread-like lines in the skin) or pimple-like
irritations.
• In infants, the rash can present as vesicles/fluid filled blisters.
• The scabies rash typically affects the hands, the webbing between fingers, skin
folds at the wrists,
• knees, elbows, underarms, waist or buttocks; the genitalia; the breasts/nipples;
and the shoulder blades
• In children younger than 2 years old, the rash can extend to the neck, head,
palms, and soles of the feet
• Due to the vigorous scratching caused by the itching, scratch marks may cover
up the typical appearance of the rash.

Treatment
• Once diagnosed, it is essential that scabies treatment is properly completed.
With proper treatment, the rash and intense itching of scabies usually begins to
subside
• within one to two days, although some milder itching can persist for a few
weeks post treatment
• No new burrows or rashes should appear 24-48 hours after effective treatment
• The choice of a specific medication is influenced by a person’s age, pregnancy
status, the presence of coexisting skin conditions and medical history
• When treating scabies infestations, always follow the directions provided by
your physician or in the package insert.
• All products must be used strictly in accordance with label directions to
• ensure effectiveness and prevent adverse reactions from overuse or misuse

• Recommended Treatment:
• 5% permethrin cream (Elimite®)
• The recommended treatment for scabies infestation is the topical use of a 5%
• permethrin cream which is applied to the body from the neck down in a thin layer.
• The cream should then be washed off 8 to 14 hours later.
• Permethrin kills the scabies mite and eggs.
• Two (or more) applications, each about a week apart, may be necessary to eliminate all
mites
• particularly when treating crusted (Norwegian) scabies.
• This is the preferred treatment for scabies infestation in children 2 months or older
• Alternative treatments: 1% Lindane lotion ** USE WITH EXTREME CAUTION, Ivermectin,
Crotamiton lotion 10% and Crotamiton cream 10% (Eurax®, Crotan®), Precipitated sulfur 6%
in petrolatum

Topical Fungal infections
• Tinea infections are superficial fungal infections caused by three species of fungi collectively
known as dermatophytes.
• Commonly these infections are named for the body part affected, including tinea corporis
(general skin), tinea cruris (groin), and tinea pedis (feet).
• Accurate diagnosis is necessary for effective treatment.
• Diagnosis is usually based on history and clinical appearance plus direct microscopy of a
potassium hydroxide preparation.
• Culture or histologic examination is rarely required for diagnosis.
• Treatment requires attention to exacerbating factors such as skin moisture and choosing an
appropriate antifungal agent.
• Topical therapy is generally successful unless the infection covers an extensive area or is
resistant to initial therapy
• In these cases, systemic therapy may be required.
• Tinea corporis and cruris infections are usually treated for two weeks, while tinea pedis
• is treated for four weeks with an azole or for one to two weeks with allylamine medication.

• The three genera of dermatophytes, Trichophyton, Epidermophyton
Microsporum
• With some pertinent exceptions, dermatomycosis is typically confined to the
superficial keratinized tissue
• Thus, can often be treated with topical antifungal medications
• Because these agents do not penetrate hair or nails, tinea capitis, tinea
barbae, and tinea unguium usually require systemic therapy
• Trichophyton rubrum is the most common pathogen causing
dermatomycoses, including tinea pedis, tinea corporis, and tinea cruris.
• the most common are tinea pedis, tinea corporis, and tinea cruris

TINEA CORPORIS
• Tinea corporis refers to tinea anywhere on the body except the scalp, beard,
feet, or hands.
• This lesion presents as an annular plaque with a slightly raised and often scaly,
advancing border and is commonly known as ringworm.
• Each lesion may have one or several concentric rings with red papules or
plaques in the center
• As the lesion progresses, the center may clear, leaving post-inflammatory
hypopigmentation or hyperpigmentation

TINEA CRURIS
• Because it affects the groin area, tinea cruris is also known as “jock itch.” It is
characterized by red scaling plaques on the medial thighs and inguinal folds
• The plaques are typically bilateral but usually spare the penis and scrotum, in
contrast to candidiasis.
• Many people with tinea cruris have coincident tinea pedis, and it has been
postulated that the tinea cruris is spread by hand from the tinea pedis.
Tinea cruris with bilateral scaly patches on the inner thighs,
sparing the penis

TINEA PEDIS
• Tinea pedis, or athlete’s foot, is the most common dermatophyte infection
• Its etiology is closely tied to the use of occlusive footwear
• Most commonly, tinea pedis presents with toe-web maceration.
• This fairly subtle presentation is contrasted with the moccasin distribution affecting the
soles and lateral feet that is often seen in patients with T. rubrum infection
• In the latter cases, the feet tend to be hyperkeratotic with scale and some erythema
• In some cases of tinea pedis, a dermatophytid (also known as “id”) reaction may occur in
which small vesicles or pustules appear at distant sites.
• The id reaction may be the only manifestation of an otherwise asymptomatic web space
maceration and usually resolves with treatment of the primary fungal infection

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PARASITIC DISEASES.pptx