Malaria

• Malaria is a mosquito-borne infectious disease affecting

humans and other animals caused by parasitic protozoans (a
group of single-celled microorganisms) belonging to the
Plasmodium type

• he disease is most commonly transmitted by an infected

female Anopheles mosquito. The mosquito bite introduces
the parasites from the mosquito's saliva into a person's blood
• The parasites travel to the liver where they mature and
reproduce.
• Five species of Plasmodium can infect and be spread by
humans.Most deaths are caused by P. falciparum because P.
vivax, P. ovale, and P. malariae generally cause a milder form
of malaria. The species P. knowlesi rarely causes disease in
humans
• Other modes of transmission:
 From mother to unborn child
 Through blood transfusions
 Signs and symptoms
• he signs and symptoms of malaria typically begin 8–25 days
following infection
• he presentation may include headache, fever, shivering, joint
pain, vomiting, hemolytic anemia, jaundice, hemoglobin in
the urine, retinal damage, and convulsions

• The classic symptom of malaria is paroxysm—a cyclical

occurrence of sudden coldness followed by shivering and then
fever and sweating, occurring every two days (tertian fever) in
P. vivax and P. ovale infections, and every three days (quartan
fever) for P. malariae. P. falciparum infection can cause
recurrent fever every 36–48 hours, or a less pronounced and
almost continuous fever.
• Severe malaria is usually caused by P. falciparum (often
referred to as falciparum malaria)
 Complications
• respiratory distress(metabolic acidosis, noncardiogenic
pulmonary oedema, concomitant pneumonia, and severe
anaemia)
• Renal failure is a feature of blackwater fever, where
hemoglobin from lysed red blood cells leaks into the urine.
• cerebral malaria
• Enlarged spleen, enlarged liver
• low blood sugar
• spontaneous bleeding, coagulopathy, and shock
• Malaria in pregnant women is an important cause of
stillbirths, infant mortality, abortion and low birth weight
The life cycle of malaria parasites. A mosquito causes an infection by a bite. First, sporozoites enter the bloodstream, and migrate
to the liver. They infect liver cells, where they multiply into merozoites, rupture the liver cells, and return to the bloodstream. The
merozoites infect red blood cells, where they develop into ring forms, trophozoites and schizonts that in turn produce further
merozoites. Sexual forms are also produced, which, if taken up by a mosquito, will infect the insect and continue the life cycle.
 Diagnosis
• diagnosis of malaria in non-endemic areas requires a high
degree of suspicion, which might be elicited by any of the
following: recent travel history, enlarged spleen, fever, low
number of platelets in the blood, and higher-than-normal
levels of bilirubin in the blood combined with a normal level
of white blood cells.
• microscopic examination of blood films
• antigen-based rapid diagnostic tests
Ring-forms and gametocytes of he blood film is the gold standard for
Plasmodium falciparum in human blood malaria diagnosis.
 Immunity can wane
• Residents of a malaria region may be exposed to the disease
so frequently that they acquire a partial immunity, which can
lessen the severity of malaria symptoms. However, this partial
immunity can disappear if you move to a country where
you're no longer frequently exposed to the parasite.
 Treatment
• Simple or uncomplicated malaria may be treated with oral
medications.
• The most effective treatment for P. falciparum infection is the
use of artemisinins in combination with other antimalarials
(known as artemisinin-combination therapy, or ACT)
• amodiaquine, lumefantrine, mefloquine or
sulfadoxine/pyrimethamine.
• Another recommended combination is dihydroartemisinin
and piperaquine.
• the WHO recommends the use of quinine plus clindamycin
early in the pregnancy (1st trimester)
• Severe and complicated malaria are medical emergencies
since mortality rates are high (10% to 50%)
• Recommended treatment for severe malaria is the
intravenous use of antimalarial drugs.
• For severe malaria, parenteral artesunate was superior to
quinine in both children and adults.
Giardiasis
 Objectives
• How human get an infection
• Site of intestine affected by Giardia
• What are the symptomes
• How to diagnosed Giardia and what the best
test
• How to treat
• is a parasitic disease caused by Giardia
lamblia.
• usually spreads when Giardia lamblia cysts
within feces contaminate food or water which
is then eaten or drunk.
• It may also spread between people and from
other animals.
• Cysts may survive for nearly three months in
cold water
• Giardia organisms infecting the cells of the
duodenum and jejunum of the small intestine
• The attachment of trophozoites causes villus
flattening and inhibition of enzymes that
break down disaccharide sugars
• uses enzymes that break down proteins
 Signs and symptoms
• Symptoms typically develop 10 days to 3 weeks
• Either asymptomatic,acute,chronic
• Diarrhea is the most common symptom of acute Giardia
infection, occurring in 90% of symptomatic subjects.
Abdominal cramping, bloating, and flatulence occur in
70-75% of symptomatic patients
• Most people are asymptomatic; only about a third of
those infected exhibit symptoms.
• Nausea
• Malodorous, greasy stools
• Anorexia
• Weight loss
• Vomiting
• Symptomatic infections are well recognized as
causing lactose intolerance
• Vomiting,blood in the stool, and fever are
innfrequent
 Diagnosis

• According to the CDC, detection of antigens on the

surface of organisms in stool specimens is the current
test of choice which provides increased sensitivity over
more common microscopy techniques

• Microscopic examination of the stool for motile

trophozoites or for the distinctive oval G.lamblia cysts

• entero-test uses a gelatin capsule

 treatment
• When symptoms are present treatment is
typically with either tinidazole or
metronidazole, nitazoxanide
• People may become temporarily lactose
intolerant after an infection and therefore it is
often recommended milk be avoided for a few
weeks.
Amebiasis
 objectives
• What are the different kinds of entamoeba
• What are the intestinal and extra intestinal
manifestation
• How to diagnose Entamoeba
• What are the differential diagnosis
• How to treat
• Amebiasis is defined as infection with Entamoeba histolytica
• Infections range from asymptomatic colonization to amebic
colitis and life-threatening abscesses.
• disease may occur months to years after exposure.
• 2 morphologically identical but genetically distinct and
apparently nonpathogenic Entamoeba species are now
recognized as causing most asymptomatic cases(DISPAR,
MOSHKOVSKII).
• E histolytica begins when infectious cysts are ingested in
fecally contaminated food or water
• People in highly endemic areas probably have recurrent
asymptomatic infections
• In developed countries, amebic colitis is most commonly
found in travelers to or emigrants from endemic countries
institutionalized persons, and patients infected with human
immunodeficiency virus.
• invasive intestinal disease may occur days to years after initial
infection and is characterized classically by abdominal pain
and bloody diarrhea and (rarely) fever
• Watery or mucus-containing diarrhea, constipation, and
tenesmus may also occur.
• trophozoites invading and laterally undermining the intestinal
surface to form the so-called flask-shaped ulcers
• The right side of the colon is commonly involved.
• Patients at increased risk of severe disease include those who
are very young, very old, malnourished, or pregnant and
those who are receiving corticosteroids
• Complications of intestinal disease
• Extensive fulminant necrotizing colitis
• stricture,
• rectovaginal fistulas
• formation of an annular intraluminal mass (ameboma),
• bowel obstruction,
• perianal skin ulceration,
• toxic megacolon,
• perforation, peritonitis, shock, and death
• Chronic intestinal amebiasis is also well described; patients
with this condition can have years of intermittent abdominal
pain, diarrhea, and weight loss.
• On rare occasions, E histolytica trophozoites enter the
bloodstream and disseminate to other body sites
• most commonly the liver via spread from the intestine
through the portal vein. The right lobe is 4 times more likely
to be involved than the left with formation of microabscess
• Most patients (65%-75%) present with a single abscess
• tender hepatomegaly and pain in the right upper quadrant.
• Unlike amebic colitis, ALA is commonly accompanied by fever,
as well as by rigors, chills, and profuse sweating
• Most patients do not have concurrent colitis and cysts, and
trophozoites are not always seen on fecal smears
• Jaundice is not typically present;
• elevated bilirubin levels are seen in less than 50% of patients,
• elevated alkaline phosphatase levels are common
• complications include secondary bacterial infection;
perforation into peritoneal, pleural, and pericardial cavities;
septic shock; and death.
• Rarely, trophozoites end up in other regions of the body, such
as the brain, spleen, lungs, and genitourinary tract
 DIAGNOSIS
• linically, it is desirable to definitively distinguish E histolytica
from E dispar and E moshkovskii because, of the 3, it is the
only proven human pathogen
• The diagnosis of invasive amebiasis is usually suggested by the
patient's presenting symptoms, exposure history, and
radiologic findings but should be confirmed with
microbiological laboratory results
• Light microscopic examination of fecal specimens (ie, “ova and
parasite” examination)
• he characteristic trophozoites and cysts can often be
identified through direct, concentrated, and/or permanently
stained smears
• Because organisms may appear intermittently, current
recommendations call for submission of 3 stool specimens on
different days during a period of 10 days
• stool specimens from patients with disseminated disease may
not contain cysts and trophozoites, despite repeated
examinations.
• if stool cannot be examined in the fresh state (within 15
minutes) for motile trophozoites, then it should be placed
immediately in an appropriate fixative to prevent
deterioration of organisms
• Unfortunately, microscopy alone cannot differentiate E
histolytica from E dispar and E moshkovskii; additional tests
are required for definitive speciation
• he rare exception is when trophozoites containing ingested
red blood cells are identified; they are strongly (but not
definitively) indicative of invasive amebiasis
• Trophozoites may also be identified in intestinal biopsy
specimens, scrapings, or aspirates, allowing a diagnosis of
amebiasis to be made if mucosal invasion and ulceration are
also observed.
• WHO/PAHO recommends that morphologically consistent
cysts and trophozoites receive the nonspecific diagnosis E
histolytica/E dispa,and the clinician must then interpret this
laboratory result in the context of the individual patient and
determine whether treatment is warranted.
• Serologic tests detect the presence of species-specific antibodies in
the patient's serum
 have a good sensitivity and specificity for detecting invasive
intestinal disease
 test of choice for ALA because titers are typically high and test
sensitivities and specificities exceed 95%
 cannot distinguish between past and current infection unless IgM is
detected;
• Fecal antigen detection tests use specific monoclonal or polyclonal
antibodies to detect E histolytica .this test rapid, highly sensitive,
useful for confirming microscopic findings and providing a diagnosis
in patients with negative fecal smear
• The highest sensitivity and specificity for the diagnosis of E
histolytica are offered by DNA-based tests
 DIFFERENTIAL DIAGNOSIS
• bacterial (eg, Salmonella and Shigella spp, Mycobacterium
tuberculosis),
• parasitic (eg, Schistosoma mansoni, Balantidium coli),
• noninfectious (eg, inflammatory bowel disease, carcinoma,
ischemic colitis, diverticulitis)
• amebomas may mimic carcinoma, tuberculosis, or an
appendiceal mass.
• the diagnosis of ALA may not be straightforward. The
differential diagnosis includes bacterial abscess, echinococcal
cyst, tuberculosis, and primary or metastatic tumor,
Toxoplasmosis
• A parasticc disease caused by Toxoplasma gondii
• Toxoplasmosis is usually spread by eating poorly cooked food
that contains cysts, exposure to infected cat feces, and from a
mother to a child during pregnancy if the mother becomes
infected. Rarely the disease may be spread by a blood
transfusion
• Up to half of the world's population are infected by
toxoplasmosis but have no symptomes
 Acute toxoplasmosis

• is often asymptomatic in healthy adults.

• The toxoplasmic trophozoites causing acute toxoplasmosis are
referred to as tachyzoites, and are typically found in bodily
fluids
• symptoms may manifest and are often influenza-like , swollen
lymphnodes , headaches, fever, and fatigue or muscle aches
and pains that last for a month or more
• Rarely will a human with a fully functioning immune system
develop severe symptoms following infection.
• Young children and immuncompromised people, such as
those with HIV/AIDS, those taking certain types of
chenmotherapy, or those who have recently received an
organ transplant, may develop severe toxoplasmosis
• This can cause damage to the brain (encephalitis) or the eyes
(necrotizing retinochoroditis), , lung problems that may
resemble tuberculosis or Pneumocysti
 Latent toxoplasmosis

• In most immuncompetent people, the infection enters a

latent phase, during which only bradyzoites (tissue cysts) are
present
• these tissue cysts and even lesions can occur in the retinas,
alveolar lining of the lungs , heart, skeletal muscle, and the
central nervous system (CNS), including the brain
 Congenital toxoplasmosis
• Congenital toxoplasmosis is associated with fetal death and
abortion, and in infants, it is associated with neurologic
deficits, neurocognitive deficits, and chorioretinitis
• A positive antibody titer indicates previous exposure and
immunity, and largely ensures the unborn fetus' safety.
• If a woman receives her first exposure to T. gondii while
pregnant, the fetus is at particular risk.
 Diagnosis

• serological testing can detect T. gondii antibodies in the

blood serum which measure IgG antibody
• IgG antibodies usually appear within a week or two of
infection, peak within one to two months, then decline at
various rates
• Toxoplasma IgG antibodies generally persist for life, and
therefore may be present in the bloodstream as a result
of either current or previous infectio
• IgM antibodies can be used to detect acute infection, but
generally not chronic infection
• The IgM antibodies appear sooner after infection
(approximately a week)than the IgG antibodies and disappear
faster than IgG antibodies after recovery(within one to six
months)
• T. gondii may also be detected in blood, amniotic fluid, or
cerebrospinal fluid by using polymerase chain reaction
• prenatal diagnosis based on testing of amniotic fluid and
ultrasound examinations;

• neonatal diagnosis based on molecular testing of placenta and

cord blood and comparative mother-child serologic tests and
a clinical examination at birth; and early childhood diagnosis
based on neurological and opthalmological examinations and
a serologic survey during the first year of life
 Treatment

• Treatment is often only recommended for

people with serious health problems, such as
people with HIV whose CD4 counts are under
200 cells/mm
• Trimethoprim/sulfamethoxazole is the drug of
choice to prevent toxoplasmosis, but not for
treating active disease
 Acute infection
• Pyrimethamine
• Sulfadiazine used in combination with pyrimethamine
to treat toxoplasmosis Combination therapy is usually
given with folic acid supplements to reduce incidence
of thrmbocytopenia.
• Combination therapy is most useful in the setting of
HIV.
• Clindamycin
• Spiramycin — an antibiotic used most often for
pregnant women to prevent the infection of their
children
 latent
• In people with latent toxoplasmosis, the cysts are
immune to these treatments, as the antibiotics do
not reach the bradyzoites in sufficient concentration.
• Atovaquone — an antibiotic that has been used to
kill Toxoplasma cysts inside AIDS patient
• Clindamycin — an antibiotic that, in combination
with atovaquone, seemed to optimally kill cysts in
mic