Parasitology-lec 12 Trypanosomes
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PARASITOLOGY LECTURE 12 – Trypanosomes and Coccidia Lecture and Notes by Dr. Llanera/Dr. Lagamayo USTMED ’07 Sec C – AsM TRYPANOSOMOA SPECIES Trypanosoma species responsible for human diseases
TRYPANOSOMA BRUCEI sspp RHODESIENSE (East African sleeping sickness)
• •
No morphologic difference with T. gambiense Lower over all prevalence
•
Rates of infectious to non-infectious fly vector 1:534(host valleys); 1:1312 (cool plateau) with suspicion of other blood sucking insects as transmitters Reservoir in game animals
• Group Complex
•
Toxic – characteristically more rapid and fulminant, reaches climax before any considerable nervous system involvement
PATHOGENESIS
• TRYPANOSOMA BRUCEI sspp GAMBIENSE
• •
Habitat – blood and various tissues Vector and Intermediate host o Glosina flies (palpalis) both males and females
LIFE CYCLE OF TRYPANOSOMA BRUCEI
•
Local infiltration from area of bite to the lymphatics and endothelial cells to arachnoid spaces and CNS Chronic inflammation of the lymphatics and perivascular infiltration and with pressure and hemorrhage creating atrophy of dendrons in ganglion cells
SYMPTOMATOLOGY
• • •
Incubation period – asymptomatic (2-23 days) Invasion of lymph nodes – (variable duration) , Winterbottoms sign, Kerandels sign, localized edema, alternating febrile attacks Invasion of the nervous system – headaches, gradual development of mental dullness, apathy, initially excitable or morose then eventually asthenia and death
DIAGNOSIS
• • •
Characteristic symptoms in endemic areas Demonstration of parasite in blood tissues on CSF Serology (for large scale screening) ELISA, IF
PROGNOSIS
• •
Good if diagnosed early Poor with CNS involvement
TREATMENT
• •
General supportive measures Drug Treatment o Pentamidine o Suramin o Melarsopenol o Tryparsamide o Melarsen
PREVENTION
• • EPIDEMIOLOGY
•
Limited to tropical West and Central Africa correlating to the range of fly vector (shaded stream banks)
•
Workers in such areas are at risks
•
Less than 10% of flies become infective after biting an infected patients Congenital transmission possible Reservoir host – domestic animals, no proof in game animals, though experimental infection have been proven
•
Treatment of cases Elimination of vectors o Spray o Clearing of vegetations o Application of mass treatment and prophylaxis Development of good control programs by trained personnel
TRYPANOSOMA CRUZI (Chaga’s Disease, S. American Trypanosomiasis)
• •
Trypanosoma Brucei Gambiense
•
Mode of transmission o From feces of arthropod containing metacyclic trypomastigotes o Transplacental o Accidental ingestion o Blood transfusion
EPIDEMIOLOGY
• •
• •
Zoonosis in moist warm regions of Western hemisphere Reservoir in wild mammals Vectors – triatomid bugs (Panstrongylus, Triatomid, Rhodnius) Affects low income groups in suburban and rural localities
•
Most frequent in children
PATHOGENESIS
•
Engulfed by histiocytes and multiply as amastigotes and invade adipose tissues. An inflammatory response follows with infiltration of PMNs, monocytes and lymphocytes with eventual fibrotic encapsulation to form a primary lesionà chagoma. From primary site – metastasize to regional lymph nodes later to the blood stream and multiples in fixed histocytes in various organs
• •
Elimination of bugs – insecticides – gammexane Education of families in endemic areas
Trypanosoma cruzi in skeletal muscle
Trypanosoma cruzi
PATHOLOGY
•
Destruction of RE and other tissue cells with predilection to mesenchynol cells (adipose, myocardial, RE, neurologlial)
COCCIDIA
•
LIFE CYCLE OF TRYPANOSMA CRUZI
• •
Early 1970sfirst discovery of Toxoplasma gondii parasite as a coccidia and the cat was the definitive host Sexual stage in the life cycle of this parasite had an important epidemiologic implication Early 1980s- Cryptosporidia causes an opportunistic infection causing diarrhea
COMMON FEATURES OF COCCIDIA
• • •
Sexual stage in the intestinal mucosa of a carnivorous definitive host Oocyst or sporocyst passes out of the feces to infect the intermediate host asexual multiplication of parasite Cryptosporidium, Isospora, and Eimeria o Single host - both sexual and asexual stages of multiplication occurs
TOXOPLASMA GONDII HISTORY
• • •
1908 - T. gondii was first found in African rodent Ctenodactylus gondii 1923 - Janku described toxoplasmic chorioretinitis 1939 - Wolf et al isolated the parasite and established the cause of congenital neonatal disease
MORPHOLOGY OF T. GONDII
•
o
SYMPTOMATOLOGY
• • •
Acute form – high fever, generalized or local edema (Romana’s sign) lipochagomas) Sub-acute stage – hepatosplenomegaly, general glandular enlargement Chronic stage – mostly in adults myxedema, megaesophagus, dyshagia, paraphlegia, etc.
DIAGNOSIS
• • • • •
Blood smear Serology – complement fixation (specific and practical) Xenodiagnosis Excision biopsy of chagomas Differential Diagnosis o Primary lesions – allergic skin lesions o Acute stage – typhoid, rheumatic fever, acute leukemoid, etc. o Chronic stage – primary cardiomyopathy, ASHD, CA of colon, hypothyroidism
In Man
o •
Bradyzoites - collection of tachyzoites in the host cell with parasite membrane measures 10 to 100 um in diameter Cyst - contains 50 to several thousands of bradyzoites
In CATs’ intestinal epithelium: o male and female gametocytes o fertilized gametocytes spherical oocysts (1013 u) rupture out of the intestinal epithelial cells passed out of the cats’ feces o oocyst develop into 2 sporocysts o each sporocyst contains 4 sporozoites
Toxoplasma gondii
TREATMENT
• • • •
8-amino quinolones – primaquine reduce parasitemia but with no evidence of its effect on the ultimate course of disease Bayer 2502 (Nifurtomax) Symptomatic and supportive treatment Surgery
PROGNOSIS
•
11.7% fatality in acute cases
PREVENTION
LIFE CYCLE OF T. GONDII
• •
Endodygeny- a tachozoite forms 2 daughter cells within a mother cell Tachozoite: o consume O2 o respiration is cyanide sensitive o Use dextrose o evolve CO2 o grows in mammalian or avian organs or tissues (brain, eye, skeletal muscles) o cannot synthesize purines
Transmission cycle of Toxoplasma gondii
o Hydrocephaly o Microcephaly o Psychomotor disturbances o Convulsions o Visceral and muscular lesions • Acquired or Reactivated Toxoplasmosis Clinical types of acquired post-natal toxoplasmosis: 1. Mild lymphatic form - resembles Infectious Mononucleosis cervical and axillary lymphadenopathy malaise, muscle pain, irregular low grade fever, slight anemia, low BP, leukopenia, lymphocytosis, slightly altered liver function 2. Acute Fulminating, disseminated Infections skin rash meningoencephalitis - high grade fever hepatitis pneumonitis chills myocarditis prostration PATHOLOGY AND SYMPTOMATOLOGY
1980’s • Toxoplasmic encephalitits as a complication of AIDS • CNS infection with Toxoplasma: o headache o altered mental status o fever o lethargy o focal neurologic deficits o convulsions DIAGNOSIS OF TOXOPLASMOSIS
•
Serologic Tests: o IgM antibodies by double-sandwhich ELISA o Indirect fluorescent antibody (IFA) for IgG and IgM determination o ELISA and IHA o PCR detection of Toxo DNA o Mice / tissue inoculation with clinical specimens
Toxoplasma gondii. Cyst in H & E stained tissue section of mouse brain
Giemsa stained cyst in an impression smear
Giemsa – stained trophozoites in peritoneal fluid of mouse called Tachyzoites found in tissues and fluids during the acute stage of infection.
EPIDEMIOLOGY
• • •
•
Toxoplasmosis is cosmopolitan Antibody vs. T.gondii: 20% to 75% of various populations are chronically ill but asymptomatic France: Raw meat as a gourmet and “health food” for children – serology rate is higher in both adults and children Congenital infection is acquired by transplacental transmission from mothers who were infected during pregnancy
PATHOLOGY AND SYMPTOMATOLOGY
•
Congenital Toxoplasmosis o 1-5/1000 pregnancies o Intracerebral calcification o Chorioretinitis
Giemsa – stained trophozoites in tissue culture Macrophage infected with Toxoplasma gondii: tachyzoites form rosette in the parasitophorous vacuole within the infected cell
TREATMENT OF TOXOPLASMOSIS
•
• •
Symptomatic infections: o pyrimethamine (Daraprim) Adult: 25-50 mg per day orally x 3-4 weeks o trisulfapyrimidines, 2-6 g per day orally x 3-4 weeks Pregnant women: o spiramycin o clindamycin AIDS patients: o Atovaquone- toxoplasmic encephalitis
PREVENTIVE MEASURES FOR TOXOPLASMOSIS
•
• • • •
Thorough cooking of all meats Careful attention to cats’ feces (sporozoites remain infective up to 18 months in the soil) Avoid tasting raw meat and wash hands with soap and water after handling meat Keep cats in houses where there are no rodents ( feed cats dry or cooked canned cat food) Empty litter box daily; disinfect with boiling water and wash hands after
ISOSPORA BELLI
• • • •
Only known coccidial parasite for which MAN is the DEFINITIVE HOST Sexual multiplication takes place in the intestinal mucosa Geographic distribution: Central and South America, Africa, Southeast Asia, Chile An opportunistic infection in AIDS patients
•
• •
MORPHOLOGY
•
PATHOLOGY AND SYMPTOMATOLOGY
Oocysts : forms found in the stool o elongated or ovoid o 25 to 33 u by 12 to 16 u in size o in fresh feces: granular cytoplasm with smooth, colorless, two-layered wall, unsegmented or unsporulated
excretion of oocysyts in healthy and symptomatic (diarrhea) individuals Malabsorption syndrome, weight loss, even fatal outcome Biopsy: shortened villi, hypertrophied crypts, infiltration of lamina propria, with eosinophils, polys, and round cells
DIAGNOSIS
•
oocysts in the feces
•
oocysts and/or sporocysts in duodenal contents Intracellular stages of the parasite in intestinal biopsies
•
Isospora belli
Isospora belli, immature oocyst (Diagnostic stage in stool specimens)
Unicellular oocyt
Oocyst w/ 2 Sporoblasts
LIFE CYCLE OF ISOSPORA BELLI
Oocyst with 2 spores each containing 4 sporozoites
TREATMENT
•
• •
Mild and asymptomatic infections: o rest o bland diet Combined: pyrimethamine( 75 mg) and sulfadiazide (4 g) or Trimetoprim- sulfamethoxazole (160 mg with 800 mg, respectively) for 10 days for AIDS pxs: low doses for longer period
CRYPTOSPORIDIUM
• • •
Protozoa parasite of the subclass Coccidia (C. parvum) Human cryptosporidiosis is worldwide in distribution Causes diarrhea in travelers, in day care centers and in water-borne outbreaks
SIGNS AND SYMPTOMS
• • • •
Diarrhea Nausea Vomiting abdominal cramps
•
fever
PATHOLOGY
•
Small intestines; stomach and colon may also be involved
DIAGNOSIS
• •
• • •
up to 100/min; cyanosis Older children and adults: rapid onset with fever, rapid respiration, non-productive cough, and cyanosis. Radiographs show diffuse infiltrates, bilateral, has a ground glass appearance Death due to asphyxia
DIAGNOSIS
stool exam: basic and modified Acid Fast stain Concentration procedures: o sucrose flotation o formalin-ether method o formalin-ethyl acetate method
LIFE CYCLE OF CRYPTOSPORIDIUM PARVUM
• • • • •
Surgical open lung biopsy for tissue imprints and tissue sections Bronchoalveolar lavage fluid Bronchoscopy for brush biopsy specimen Aspiration lung biopsy; tracheal aspirates Laboratory tests o Toluidine or methenamine silver stains o Monoclonal antibodies o Serologic tests for antibody to P.carinii
Pneumocystis carinii
Gomori methenamine-silver nitrate stain: Cysts in human lung section: cup-shape appearance due to partial collapse of the cyst wall
Cysts in human lung impression smear Carinii (silver nitrate) H & E section of human lung. Alveioli appear to be filled with pinkstaining, foamy material.
TREATMENT
• •
Neither cysts nor organisms can be seen in this stain
Long list of antibiotics are ineffective Spiramycin(?) 1g TID x 2 weeks
PREVENTION
• • •
avoid contact with infected materials use gloves, gowns and hand washing full strength commercial bleach(5% NaHypochlorite) or 5 to 10% household NH4
PNEUMOCYSTIS CARINII
• •
• • •
An extracellular organism causing interstitial pneumonia (protozoa-?) By sequence analysis of ribosomal RNA, it is closely related to fungi Morphology: unicellular, pleomorphic, 1-2 u in diameter; tropozoites up to 5 u; cysts -spherical or crescentic, thick-walled structure, 4-6 u in diameter Exact multiplication of the organism is unknown Transmission: droplet to close contacts
EPIDEMIOLOGY
• •
•
cosmopolitan in humans, rodents, dogs, and other domestic animals Fatal pneumonia in premature and malnourished infants In older children and adults: associated with hypogammaglobulinemia, leukemia, Hodgkin’s lymphoma, malignancies,use of corticosteroids AIDS patients
PATHOLOGY
• •
Lungs- firm ; cut surface areas are gray and airless Microscopic: thickened alveolar septa, infiltrated with plasma cells (interstitial plasma cell pneumonia) o alveolar epithelium- partially desquamated o alveoli- filled with fat laden cells, parasites and foamy, vacuolated material
SYMPTOMATOLOGY
•
Infantile disease: insidious onset for over weeks with poor feeding o failure to thrive; rapid respiratory rate of
TREATMENT
•
•
•
Combination of trimethoprim - sulfamethoxazole (Bactrim) o 120 mg per kg per day, every 6 hrs x 14 days for adults and children Prophylaxis in high risk pxs.: 5 and 25 mg per kg per day divided into 2 equal doses at 12 hrs intervals AIDS patients: inhalation of aerosolized pentamidine
HAPPY HEARTS’ DAY! ♥♥♥♥♥ [email protected] [email protected]
TRYPANOSOMA BRUCEI sspp RHODESIENSE (East African sleeping sickness)
• •
No morphologic difference with T. gambiense Lower over all prevalence
•
Rates of infectious to non-infectious fly vector 1:534(host valleys); 1:1312 (cool plateau) with suspicion of other blood sucking insects as transmitters Reservoir in game animals
• Group Complex
•
Toxic – characteristically more rapid and fulminant, reaches climax before any considerable nervous system involvement
PATHOGENESIS
• TRYPANOSOMA BRUCEI sspp GAMBIENSE
• •
Habitat – blood and various tissues Vector and Intermediate host o Glosina flies (palpalis) both males and females
LIFE CYCLE OF TRYPANOSOMA BRUCEI
•
Local infiltration from area of bite to the lymphatics and endothelial cells to arachnoid spaces and CNS Chronic inflammation of the lymphatics and perivascular infiltration and with pressure and hemorrhage creating atrophy of dendrons in ganglion cells
SYMPTOMATOLOGY
• • •
Incubation period – asymptomatic (2-23 days) Invasion of lymph nodes – (variable duration) , Winterbottoms sign, Kerandels sign, localized edema, alternating febrile attacks Invasion of the nervous system – headaches, gradual development of mental dullness, apathy, initially excitable or morose then eventually asthenia and death
DIAGNOSIS
• • •
Characteristic symptoms in endemic areas Demonstration of parasite in blood tissues on CSF Serology (for large scale screening) ELISA, IF
PROGNOSIS
• •
Good if diagnosed early Poor with CNS involvement
TREATMENT
• •
General supportive measures Drug Treatment o Pentamidine o Suramin o Melarsopenol o Tryparsamide o Melarsen
PREVENTION
• • EPIDEMIOLOGY
•
Limited to tropical West and Central Africa correlating to the range of fly vector (shaded stream banks)
•
Workers in such areas are at risks
•
Less than 10% of flies become infective after biting an infected patients Congenital transmission possible Reservoir host – domestic animals, no proof in game animals, though experimental infection have been proven
•
Treatment of cases Elimination of vectors o Spray o Clearing of vegetations o Application of mass treatment and prophylaxis Development of good control programs by trained personnel
TRYPANOSOMA CRUZI (Chaga’s Disease, S. American Trypanosomiasis)
• •
Trypanosoma Brucei Gambiense
•
Mode of transmission o From feces of arthropod containing metacyclic trypomastigotes o Transplacental o Accidental ingestion o Blood transfusion
EPIDEMIOLOGY
• •
• •
Zoonosis in moist warm regions of Western hemisphere Reservoir in wild mammals Vectors – triatomid bugs (Panstrongylus, Triatomid, Rhodnius) Affects low income groups in suburban and rural localities
•
Most frequent in children
PATHOGENESIS
•
Engulfed by histiocytes and multiply as amastigotes and invade adipose tissues. An inflammatory response follows with infiltration of PMNs, monocytes and lymphocytes with eventual fibrotic encapsulation to form a primary lesionà chagoma. From primary site – metastasize to regional lymph nodes later to the blood stream and multiples in fixed histocytes in various organs
• •
Elimination of bugs – insecticides – gammexane Education of families in endemic areas
Trypanosoma cruzi in skeletal muscle
Trypanosoma cruzi
PATHOLOGY
•
Destruction of RE and other tissue cells with predilection to mesenchynol cells (adipose, myocardial, RE, neurologlial)
COCCIDIA
•
LIFE CYCLE OF TRYPANOSMA CRUZI
• •
Early 1970sfirst discovery of Toxoplasma gondii parasite as a coccidia and the cat was the definitive host Sexual stage in the life cycle of this parasite had an important epidemiologic implication Early 1980s- Cryptosporidia causes an opportunistic infection causing diarrhea
COMMON FEATURES OF COCCIDIA
• • •
Sexual stage in the intestinal mucosa of a carnivorous definitive host Oocyst or sporocyst passes out of the feces to infect the intermediate host asexual multiplication of parasite Cryptosporidium, Isospora, and Eimeria o Single host - both sexual and asexual stages of multiplication occurs
TOXOPLASMA GONDII HISTORY
• • •
1908 - T. gondii was first found in African rodent Ctenodactylus gondii 1923 - Janku described toxoplasmic chorioretinitis 1939 - Wolf et al isolated the parasite and established the cause of congenital neonatal disease
MORPHOLOGY OF T. GONDII
•
o
SYMPTOMATOLOGY
• • •
Acute form – high fever, generalized or local edema (Romana’s sign) lipochagomas) Sub-acute stage – hepatosplenomegaly, general glandular enlargement Chronic stage – mostly in adults myxedema, megaesophagus, dyshagia, paraphlegia, etc.
DIAGNOSIS
• • • • •
Blood smear Serology – complement fixation (specific and practical) Xenodiagnosis Excision biopsy of chagomas Differential Diagnosis o Primary lesions – allergic skin lesions o Acute stage – typhoid, rheumatic fever, acute leukemoid, etc. o Chronic stage – primary cardiomyopathy, ASHD, CA of colon, hypothyroidism
In Man
o •
Bradyzoites - collection of tachyzoites in the host cell with parasite membrane measures 10 to 100 um in diameter Cyst - contains 50 to several thousands of bradyzoites
In CATs’ intestinal epithelium: o male and female gametocytes o fertilized gametocytes spherical oocysts (1013 u) rupture out of the intestinal epithelial cells passed out of the cats’ feces o oocyst develop into 2 sporocysts o each sporocyst contains 4 sporozoites
Toxoplasma gondii
TREATMENT
• • • •
8-amino quinolones – primaquine reduce parasitemia but with no evidence of its effect on the ultimate course of disease Bayer 2502 (Nifurtomax) Symptomatic and supportive treatment Surgery
PROGNOSIS
•
11.7% fatality in acute cases
PREVENTION
LIFE CYCLE OF T. GONDII
• •
Endodygeny- a tachozoite forms 2 daughter cells within a mother cell Tachozoite: o consume O2 o respiration is cyanide sensitive o Use dextrose o evolve CO2 o grows in mammalian or avian organs or tissues (brain, eye, skeletal muscles) o cannot synthesize purines
Transmission cycle of Toxoplasma gondii
o Hydrocephaly o Microcephaly o Psychomotor disturbances o Convulsions o Visceral and muscular lesions • Acquired or Reactivated Toxoplasmosis Clinical types of acquired post-natal toxoplasmosis: 1. Mild lymphatic form - resembles Infectious Mononucleosis cervical and axillary lymphadenopathy malaise, muscle pain, irregular low grade fever, slight anemia, low BP, leukopenia, lymphocytosis, slightly altered liver function 2. Acute Fulminating, disseminated Infections skin rash meningoencephalitis - high grade fever hepatitis pneumonitis chills myocarditis prostration PATHOLOGY AND SYMPTOMATOLOGY
1980’s • Toxoplasmic encephalitits as a complication of AIDS • CNS infection with Toxoplasma: o headache o altered mental status o fever o lethargy o focal neurologic deficits o convulsions DIAGNOSIS OF TOXOPLASMOSIS
•
Serologic Tests: o IgM antibodies by double-sandwhich ELISA o Indirect fluorescent antibody (IFA) for IgG and IgM determination o ELISA and IHA o PCR detection of Toxo DNA o Mice / tissue inoculation with clinical specimens
Toxoplasma gondii. Cyst in H & E stained tissue section of mouse brain
Giemsa stained cyst in an impression smear
Giemsa – stained trophozoites in peritoneal fluid of mouse called Tachyzoites found in tissues and fluids during the acute stage of infection.
EPIDEMIOLOGY
• • •
•
Toxoplasmosis is cosmopolitan Antibody vs. T.gondii: 20% to 75% of various populations are chronically ill but asymptomatic France: Raw meat as a gourmet and “health food” for children – serology rate is higher in both adults and children Congenital infection is acquired by transplacental transmission from mothers who were infected during pregnancy
PATHOLOGY AND SYMPTOMATOLOGY
•
Congenital Toxoplasmosis o 1-5/1000 pregnancies o Intracerebral calcification o Chorioretinitis
Giemsa – stained trophozoites in tissue culture Macrophage infected with Toxoplasma gondii: tachyzoites form rosette in the parasitophorous vacuole within the infected cell
TREATMENT OF TOXOPLASMOSIS
•
• •
Symptomatic infections: o pyrimethamine (Daraprim) Adult: 25-50 mg per day orally x 3-4 weeks o trisulfapyrimidines, 2-6 g per day orally x 3-4 weeks Pregnant women: o spiramycin o clindamycin AIDS patients: o Atovaquone- toxoplasmic encephalitis
PREVENTIVE MEASURES FOR TOXOPLASMOSIS
•
• • • •
Thorough cooking of all meats Careful attention to cats’ feces (sporozoites remain infective up to 18 months in the soil) Avoid tasting raw meat and wash hands with soap and water after handling meat Keep cats in houses where there are no rodents ( feed cats dry or cooked canned cat food) Empty litter box daily; disinfect with boiling water and wash hands after
ISOSPORA BELLI
• • • •
Only known coccidial parasite for which MAN is the DEFINITIVE HOST Sexual multiplication takes place in the intestinal mucosa Geographic distribution: Central and South America, Africa, Southeast Asia, Chile An opportunistic infection in AIDS patients
•
• •
MORPHOLOGY
•
PATHOLOGY AND SYMPTOMATOLOGY
Oocysts : forms found in the stool o elongated or ovoid o 25 to 33 u by 12 to 16 u in size o in fresh feces: granular cytoplasm with smooth, colorless, two-layered wall, unsegmented or unsporulated
excretion of oocysyts in healthy and symptomatic (diarrhea) individuals Malabsorption syndrome, weight loss, even fatal outcome Biopsy: shortened villi, hypertrophied crypts, infiltration of lamina propria, with eosinophils, polys, and round cells
DIAGNOSIS
•
oocysts in the feces
•
oocysts and/or sporocysts in duodenal contents Intracellular stages of the parasite in intestinal biopsies
•
Isospora belli
Isospora belli, immature oocyst (Diagnostic stage in stool specimens)
Unicellular oocyt
Oocyst w/ 2 Sporoblasts
LIFE CYCLE OF ISOSPORA BELLI
Oocyst with 2 spores each containing 4 sporozoites
TREATMENT
•
• •
Mild and asymptomatic infections: o rest o bland diet Combined: pyrimethamine( 75 mg) and sulfadiazide (4 g) or Trimetoprim- sulfamethoxazole (160 mg with 800 mg, respectively) for 10 days for AIDS pxs: low doses for longer period
CRYPTOSPORIDIUM
• • •
Protozoa parasite of the subclass Coccidia (C. parvum) Human cryptosporidiosis is worldwide in distribution Causes diarrhea in travelers, in day care centers and in water-borne outbreaks
SIGNS AND SYMPTOMS
• • • •
Diarrhea Nausea Vomiting abdominal cramps
•
fever
PATHOLOGY
•
Small intestines; stomach and colon may also be involved
DIAGNOSIS
• •
• • •
up to 100/min; cyanosis Older children and adults: rapid onset with fever, rapid respiration, non-productive cough, and cyanosis. Radiographs show diffuse infiltrates, bilateral, has a ground glass appearance Death due to asphyxia
DIAGNOSIS
stool exam: basic and modified Acid Fast stain Concentration procedures: o sucrose flotation o formalin-ether method o formalin-ethyl acetate method
LIFE CYCLE OF CRYPTOSPORIDIUM PARVUM
• • • • •
Surgical open lung biopsy for tissue imprints and tissue sections Bronchoalveolar lavage fluid Bronchoscopy for brush biopsy specimen Aspiration lung biopsy; tracheal aspirates Laboratory tests o Toluidine or methenamine silver stains o Monoclonal antibodies o Serologic tests for antibody to P.carinii
Pneumocystis carinii
Gomori methenamine-silver nitrate stain: Cysts in human lung section: cup-shape appearance due to partial collapse of the cyst wall
Cysts in human lung impression smear Carinii (silver nitrate) H & E section of human lung. Alveioli appear to be filled with pinkstaining, foamy material.
TREATMENT
• •
Neither cysts nor organisms can be seen in this stain
Long list of antibiotics are ineffective Spiramycin(?) 1g TID x 2 weeks
PREVENTION
• • •
avoid contact with infected materials use gloves, gowns and hand washing full strength commercial bleach(5% NaHypochlorite) or 5 to 10% household NH4
PNEUMOCYSTIS CARINII
• •
• • •
An extracellular organism causing interstitial pneumonia (protozoa-?) By sequence analysis of ribosomal RNA, it is closely related to fungi Morphology: unicellular, pleomorphic, 1-2 u in diameter; tropozoites up to 5 u; cysts -spherical or crescentic, thick-walled structure, 4-6 u in diameter Exact multiplication of the organism is unknown Transmission: droplet to close contacts
EPIDEMIOLOGY
• •
•
cosmopolitan in humans, rodents, dogs, and other domestic animals Fatal pneumonia in premature and malnourished infants In older children and adults: associated with hypogammaglobulinemia, leukemia, Hodgkin’s lymphoma, malignancies,use of corticosteroids AIDS patients
PATHOLOGY
• •
Lungs- firm ; cut surface areas are gray and airless Microscopic: thickened alveolar septa, infiltrated with plasma cells (interstitial plasma cell pneumonia) o alveolar epithelium- partially desquamated o alveoli- filled with fat laden cells, parasites and foamy, vacuolated material
SYMPTOMATOLOGY
•
Infantile disease: insidious onset for over weeks with poor feeding o failure to thrive; rapid respiratory rate of
TREATMENT
•
•
•
Combination of trimethoprim - sulfamethoxazole (Bactrim) o 120 mg per kg per day, every 6 hrs x 14 days for adults and children Prophylaxis in high risk pxs.: 5 and 25 mg per kg per day divided into 2 equal doses at 12 hrs intervals AIDS patients: inhalation of aerosolized pentamidine
HAPPY HEARTS’ DAY! ♥♥♥♥♥ [email protected] [email protected]
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