Toxoplasmosis is caused by the parasite Toxoplasma gondii and can cause encephalitis and neurological disease in patients with low CD4 counts. It is diagnosed through imaging, blood tests, and sometimes brain biopsies. Treatment involves antiparasitic drugs and maintaining CD4 counts through antiretroviral therapy. Cryptosporidiosis is caused by Cryptosporidium parasites and causes diarrhea. It is transmitted through contaminated water or food. Microsporidiosis is caused by various protist parasites and can infect the gut or other organs. It is diagnosed through stool or tissue samples and treated with antiparasitic drugs and antiretroviral therapy. Isosporiasis is
Streptococcus pyogenes
Streptococcus pyogenes.jpg
S. pyogenes bacteria at 900x magnification
Scientific classification
Kingdom: Eubacteria
Phylum: Firmicutes
Class: Bacilli
Order: Lactobacillales
Family: Streptococcaceae
Genus: Streptococcus
Species: S. pyogenes
Binomial name
Streptococcus pyogenes
Rosenbach 1884
Streptococcus pyogenes is a species of Gram-positive bacteria. These bacteria are aerotolerant and an extracellular bacterium, made up of non-motile and non-sporing cocci. As expected with a streptococci, it is clinically important in human illness. It is an infrequent, but usually pathogenic, part of the skin microbiota. It is the predominant species harboring the Lancefield group A antigen, and is often called group A streptococcus (GAS). However, both Streptococcus dysgalactiae and the Streptococcus anginosus group can possess group A antigen. Group A streptococci when grown on blood agar typically produces small zones of beta-hemolysis, a complete destruction of red blood cells. (A zone size of 2–3 mm is typical.) It is thus also called group A (beta-hemolytic) streptococcus (GABHS), and can make colonies greater than 5 mm in size.[1]
Like other cocci, streptococci are round bacteria. The name is derived from Greek words meaning chain(Strepto) of berries (coccus) and pus(pyo)-forming(genes), because streptococcal cells tend to link in chains of round cells (see image) and a number of infections caused by the bacterium, produce pus. Streptococci are can be catalase positive or negative.[2] S. pyogenes can be cultured on blood agar plates. Under ideal conditions, it has an incubation period of 1 to 3 days.[3]
An estimated 700 million GAS infections occur worldwide each year. While the overall mortality rate for these infections is 0.1%, over 650,000 of the cases are severe and invasive, and have a mortality rate of 25%.[4] Early recognition and treatment are critical; diagnostic failure can result in sepsis and death.[5][6]
Streptococcus pyogenes
Streptococcus pyogenes.jpg
S. pyogenes bacteria at 900x magnification
Scientific classification
Kingdom: Eubacteria
Phylum: Firmicutes
Class: Bacilli
Order: Lactobacillales
Family: Streptococcaceae
Genus: Streptococcus
Species: S. pyogenes
Binomial name
Streptococcus pyogenes
Rosenbach 1884
Streptococcus pyogenes is a species of Gram-positive bacteria. These bacteria are aerotolerant and an extracellular bacterium, made up of non-motile and non-sporing cocci. As expected with a streptococci, it is clinically important in human illness. It is an infrequent, but usually pathogenic, part of the skin microbiota. It is the predominant species harboring the Lancefield group A antigen, and is often called group A streptococcus (GAS). However, both Streptococcus dysgalactiae and the Streptococcus anginosus group can possess group A antigen. Group A streptococci when grown on blood agar typically produces small zones of beta-hemolysis, a complete destruction of red blood cells. (A zone size of 2–3 mm is typical.) It is thus also called group A (beta-hemolytic) streptococcus (GABHS), and can make colonies greater than 5 mm in size.[1]
Like other cocci, streptococci are round bacteria. The name is derived from Greek words meaning chain(Strepto) of berries (coccus) and pus(pyo)-forming(genes), because streptococcal cells tend to link in chains of round cells (see image) and a number of infections caused by the bacterium, produce pus. Streptococci are can be catalase positive or negative.[2] S. pyogenes can be cultured on blood agar plates. Under ideal conditions, it has an incubation period of 1 to 3 days.[3]
An estimated 700 million GAS infections occur worldwide each year. While the overall mortality rate for these infections is 0.1%, over 650,000 of the cases are severe and invasive, and have a mortality rate of 25%.[4] Early recognition and treatment are critical; diagnostic failure can result in sepsis and death.[5][6]
Dengue fever is the fastest emerging arboviral infection spread
by Aedes mosquitoes with major public health consequences in
over 100 tropical and sub-tropical countries in South-East Asia,
the Western Pacific, and South and Central America. Up to 2.5
billion people globally live under the threat of dengue fever and its
severe forms—dengue hemorrhagic fever (DHF) or dengue shock
syndrome (DSS). More than 75% of these people, or approximately
1.8 billion, live in the Asia-Pacific Region. As the disease spreads to
new geographical areas, the frequency of the outbreaks is increasing
along with changing disease epidemiology. It is estimated that 50
a million cases of dengue fever occur worldwide annually and half a
million people suffering from DHF require hospitalization each year,
a very large proportion of whom (approximately 90%) are children
less than five years old. About 2.5% of those affected with dengue
die of the disease.
Dengue fever is the fastest emerging arboviral infection spread
by Aedes mosquitoes with major public health consequences in
over 100 tropical and sub-tropical countries in South-East Asia,
the Western Pacific, and South and Central America. Up to 2.5
billion people globally live under the threat of dengue fever and its
severe forms—dengue hemorrhagic fever (DHF) or dengue shock
syndrome (DSS). More than 75% of these people, or approximately
1.8 billion, live in the Asia-Pacific Region. As the disease spreads to
new geographical areas, the frequency of the outbreaks is increasing
along with changing disease epidemiology. It is estimated that 50
a million cases of dengue fever occur worldwide annually and half a
million people suffering from DHF require hospitalization each year,
a very large proportion of whom (approximately 90%) are children
less than five years old. About 2.5% of those affected with dengue
die of the disease.
Similar to OPPORTUNISTIC PARASITIC INFECTIONS.ppt (20)
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Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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2. OPPORTUNISTIC INFECTIONS AND
THEIR RELATIONSHIP TO HIV/AIDS
• OIs are signs of a declining
immune system. Most life-
threatening OIs occur when your
CD4 count is below 200
cells/mm3. OIs are the most
common cause of death for
people with HIV/AIDS.
12/04
3. Opportunistic parasitic infections
in Immunosuppressed patients
• Infections with opportunistic pathogens
were the leading cause of diarrhoea in
HIV infectedindividuals, especially, in
subjects with advanced disease.
C. partum and I.belli, were the most
common pathogens.
• Among the non opportunistic pathogens
E. histolytica/
• E. dispar seemed to contribute significantly
has shown
12/04
5. Toxoplasma gondii Encephalitis:
Epidemiology
• Caused by the T gondii, a protozoan
• Disease usually caused by reactivation of latent
tissue cysts
• Primary infection may be associated with acute
cerebral or disseminated disease
• Seroprevalence varies widely: 15% in the United
States, 75% in some European countries, higher
in some developing countries
12/04
6. Toxoplasmosis
• Toxoplasmosis is caused by the parasite
Toxoplasma gondii that can cause encephalitis
and neurological disease in patients with low
CD4 counts. The parasite is carried by cats,
birds, and other animals and is also found in
soil contaminated by cat feces and in meat,
particularly pork.
12/04
7. Toxoplasma gondii
Encephalitis: Epidemiology
• In advanced AIDS, 12-month incidence of TE
was 33% in toxoplasma seropositive patients not
on prophylaxis or ART
• Incidence and mortality lower in United States
and Europe since widespread use of prophylaxis
and potent ART
• Occurs primarily in patients with CD4 count
<200 cells/µL, especially <50 cells/µL
12/04
8. Toxoplasma gondii Encephalitis:
Epidemiology
• Primary infection acquired from
tissue cysts in undercooked meat
or ingestion of sporulated oocysts
(from cat feces) in soil, water, or
food
• No transmission by person-to-
person contact
12/04
9. Toxoplasma gondii
Encephalitis: Clinical Manifestations
• Focal encephalitis with headache, confusion,
or motor weakness and fever
• Focal neurological abnormalities, may
progress to seizures, altered mental status,
coma
• Dissemination may occur, with
retinochoroiditis, pneumonia, other organ
involvement
12/04
13. Toxoplasma gondii Encephalitis:
Diagnosis
• Imaging
– CT, MRI of brain: often
multiple contrast-
enhancing lesions,
often with edema
– PET or SPECT may
help distinguish TE
from lymphoma
• Detection of organism
(brain biopsy)
• CSF PCR not sensitive
12/04
Credit: P. Volberding, MD, UCSF Center
for HIV Information Image Library
14. Toxoplasma gondii Encephalitis:
Diagnosis
• Imaging
–CT, MRI of brain: multiple contrast-
enhancing lesions, often with edema
–PET or SPECT may help distinguish TE
from lymphoma
• Detection of organism (brain biopsy)
• CSF PCR not sensitive
12/04
15. Toxoplasma gondii
Encephalitis: Diagnosis
• Definitive diagnosis: clinical syndrome +
imaging + detection of organism (brain
biopsy)
• May initially make empiric diagnosis on
basis of clinical and radiographic
improvement to TE therapy, in absence of
a likely alternative diagnosis
– Brain biopsy if failure to respond to therapy
12/04
17. • Toxoplasmosis is treatable with aggressive
therapy, and prophylaxis is recommended for
patients with low CD4 counts (usually less
than 200). Diagnosis of this condition often
requires imaging studies (CT or MRI) of the
brain and a blood test. For more information,
see CDC’s Toxoplasmosis and You Can Prevent
Toxo.
12/04
18. Toxoplasmosis is treatable
• Toxoplasmosis is treatable with aggressive
therapy, and prophylaxis is recommended for
patients with low CD4 counts (usually less
than 200). Diagnosis of this condition often
requires imaging studies (CT or MRI) of the
brain and a blood test. For more information,
see CDC’s Toxoplasmosis and You Can Prevent
Toxoplasmosis .
12/04
19. Toxoplasma gondii
Encephalitis: Treatment
• Preferred:
–Pyrimethamine 200 mg PO first dose,
then 50 mg (weight <60 kg) to 75 mg
(≥60 kg) PO QD + sulfadiazine 1,000
mg (<60 kg) to 1,500 mg (≥60 kg) PO Q
6 hours, + leucovorin 10-20 mg PO QD
• Duration: ≥6 weeks, longer if
extensive disease or incomplete
response
12/04
20. Toxoplasma gondii Encephalitis:
Prevention of Recurrence
• Lifelong chronic maintenance therapy
(secondary prophylaxis) after completion
of initial therapy, unless immune
reconstitution on ART
– Preferred: TMP-SMX 1 DS PO QD
– Alternative: dapsone 100 mg PO QD, or
dapsone + pyrimethamine + leucovorin +/-
aerosolized pentamidine, or atovaquone
12/04
21. Toxoplasma gondii Encephalitis:
Considerations in Pregnancy
• Perinatal transmission usually occurs only with
acute maternal infection, but in advanced HIV
may occur with reactivation of chronic infection
• If primary T gondii infection during pregnancy,
consult with maternal-fetal specialist
• If symptomatic toxoplasmosis during pregnancy:
– Detailed ultrasound of fetus
– Infant should be treated
12/04
22. Cryptosporidiosis
• Cryptosporidiosis is a diarrheal disease
caused by the protozoa Cryptosporidium,
and it can become chronic for people
with low CD4 counts. Symptoms include
abdominal cramps and severe chronic
diarrhea. Treatment and antiretroviral
therapy are important. For more
information, see CDC’s Cryptosporidiosis
and You Can Prevent Cryptosporidiosis.
12/04
24. Cryptosporidiosis
• Infection with this parasite can occur
through: swallowing water that has been
contaminated with fecal material (in
swimming pools, lakes, or public water
supplies); eating uncooked food (like
oysters) that are infected; or by person-
to-person transmission, including
changing diapers or exposure to feces
during sexual contact.
12/04
25. Cryptosporidiosis: Epidemiology
• Caused by Cryptosporidium
species
–Protozoan parasites
–Infect small intestine mucosa; in
immunosuppressed patients,
also infect large intestine and
other sites
12/04
26. Cryptosporidiosis: Epidemiology
• Infection results from ingestion of oocysts
excreted in feces of infected humans or animals
– Water supplies and recreational water sources
(oocysts may withstand standard chlorination)
– Person-to-person transmission via oral-anal contact,
from infected children to adults (eg, during diapering)
• Risk greatest with CD4 count <100 cells/µL
• Incidence dramatically lower in areas with
widespread use of effective ART
12/04
27. Cryptosporidiosis:
Clinical Manifestations
• Acute or subacute onset of profuse watery,
nonbloody diarrhea, often with nausea,
vomiting, and abdominal cramping
• Fever in 1/3 of patients
• Malabsorption is common; dehydration,
malnutrition may result
• Biliary tract and pancreatic duct may be
infected, causing cholangitis and
pancreatitis
12/04
29. Cryptosporidiosis: Diagnosis
• Microscopic identification of oocysts in
stool or tissue
– Modified acid-fast and other stains
– Consider repeat stool sampling
• DFA or ELISA
• Small intestine biopsy with identification of
Cryptosporidium organisms
• Cannot be cultured
12/04
30. Cryptosporidiosis: Treatment
• ART with immune restoration (to CD4
count >100 cells/µL) results in complete
resolution
• No consistently effective antimicrobial
therapy
– Consider nitazoxanide or paromomycin
• Symptomatic treatment: antidiarrheals (eg,
loperamide, tincture of opium)
• Supportive care: hydration, nutritional
support (IV therapies may be needed)
12/04
34. Microsporidiosis: Epidemiology
• Protists,
• Many species, including Enterocytozoon
bieneusi, Encephalitozoon cuniculi,
Encephalitozoon intestinalis
• Ubiquitous, may be zoonotic and/or
waterborne
• Risk greatest with CD4 count <100 cells/µL
• Incidence dramatically lower in countries
with widespread use of effective ART
12/04
35. Microsporidiosis: Epidemiology
• Ubiquitous, may be zoonotic
and/or waterborne
• Risk greatest with CD4 <100
cells/µL
• Incidence dramatically lower in
countries with widespread use of
effective ART
12/04
36. Microsporidiosis:
• In the gut of the host the spore
germinates, it builds up osmotic
pressure until its rigid wall ruptures
at its thinnest point at the apex. The
posterior vacuole swells, forcing the
polar filament to rapidly eject the
infectious content into the cytoplasm
of the potential host..
12/04
38. Microsporidiosis:
Clinical Manifestations
• Most common: diarrheal illness
• Other manifestations: cholangitis,
hepatitis, encephalitis, ocular
infection, sinusitis, myositis,
disseminated infection
• Clinical syndromes may vary by
species
12/04
39. Microsporidiosis: Diagnosis
• Some species cannot be cultured
• Microscopic identification of stool or
tissue samples
–Selective stains
–Evaluate 3 stool samples
–Small bowel biopsy if stool studies are
negative and suspicion is high
12/04
41. Microsporidiosis in
Immunocompromised persons
• Additionally, cases of microsporidiosis in
immunocompromised persons not
infected with HIV as well as in immune
competent persons also have been
reported. The clinical manifestations of
microsporidiosis are very diverse, varying
according to the causal species with
diarrhoea being the most common.
12/04
42. Microsporidiosis: Treatment
• ART with immune restoration
(to CD4 count >100 cells/µL)
–Results in resolution of
symptoms of enteric
microsporidiosis; but does not
eliminate the microsporidia
12/04
43. Microsporidiosis: Treatment
• E bieneusi infection: no specific
antimicrobial; consider fumagillin 60 mg
PO QD (not available in United States) or
nitazoxanide
• Non-E bieneusi microsporidial infection
(other than ocular): albendazole 400 mg
PO BID
– Treat until CD4 count >200 cells/µL
• Ocular infection: fumagillin (Fumidil B) eye
drops 70 mcg/mL (indefinitely) +
albendazole 400 mg PO BID
12/04
47. Microsporidiosis:
Prevention of Recurrence
• Ocular: indefinite treatment
–May consider discontinuing
maintenance therapy in
asymptomatic patients on ART
with sustained increase in CD4
count to >200 cells/µL for ≥6
months (no data to support this
approach)
12/04
49. Isosporiasis
• Isosporiasis is a human intestinal disease
caused by the parasite Isospora belli. It is
found worldwide, especially in tropical and
subtropical areas. Infection often occurs in
immuno-compromised individuals, notably
AIDS patients, and outbreaks have been
reported in institutionalized groups in the
United States. The first documented case was
in 1915.
12/04
50. Isospora belli
• The coccidian
parasite Isospora
belli infects the
epithelial cells of the
small intestine, and
is the least common
of the three
intestinal coccidia
that infect human
12/04
51. Isospora belli
• Infection causes acute, non-bloody
diarrhea with crampy abdominal pain,
which can last for weeks and result in
malabsorption and weight loss. In
immunodepressed patients, and in
infants and children, the diarrhea can be
severe. Eosinophilia may be present
(differently from other protozoan
infections)
12/04
53. Isospora belli
• Microscopic demonstration of the
large typically shaped oocysts is the
basis for diagnosis. Because the
oocysts may be passed in small
amounts and intermittently,
repeated stool examinations and
concentration procedures are
recommended.
12/04
54. . Isospora belli.
• The oocysts can be visualized on
wet mounts by microscopy with
bright-field, differential
interference contrast (DIC), and
epifluorescence. They can also be
stained by modified acid-fast
stain.
12/04
55. Isospora belli
• Trimethoprim
sulfamethoxazole is the usual
treatment choice. See
recommendations in The
Medical Letter (Drugs for
Parasitic Infections) for
complete information.
12/04