lung parasitic infections pneumocystosis - tropy.lf1.cuni.cz parasitic infections.pdf · increased...
TRANSCRIPT
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Lung parasitic infections;
Pneumocystosis
Jarmila Kliescikova, MD
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Respiratory system
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Examination of the thorax
Inspection (globally, locally)
Percussion
Auscultation
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Laboratory examination
Sputum
Induced sputum
BAL
Pulmonary function examination
Imaging studies
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Respiratory system
Affection by parasites:
Initial port of entry
As a site of definitive multiplication and affection of host
As a transitory site of development
within host (not the port of entry)
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Site of terminal multiplication
(port of entry)
Pneumocystis jiroveci
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Pneumocystis jiroveci
(Pneumocystis carinii)
Causative agent of pneumocystic pneumonia called in honor to czech parasitologist Otta Jírovec
Fungi like microorganism belonging to the group of yeasts (Sacharomyces cerevisae)
Distribution: cosmopolite
Associated with immunodeficiency
Pneumocystis isolated from dogs, monkeys, rats, mices, cats, sheeps…
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Epidemiology
¾ of population - antibodies against P. jiroveci
Nutrition status of the population
Immunocompromised patients:
in the past 80%
at present: 10-20%
Mortality: HIV – 10-20%
Mortality increased in patients without therapy to 75-100%
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Life cycle
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Forms of organism
Trophozoite (haploid) in
vivo creating clusters
Praecyst
Cyst (8 spherical
intracystic bodies, give
rise to 8 trophozoites)
Main form responsible for
infection still not known
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Immunocompetent host
Exposition mostly at the age 3-4 years
Transmission: inhalation of infectious particles (most probably cysts)
Localisation in lungs: tight contact with type I. pneumocytes secured by presence of fibronectine
Macrophages in lungs destroy majority of pneumocysts
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Pathophysiology
Destruction of basal membrane leads to
changes in permeability of
alveoli/capillaries
Changes in rate ventilation/perfusion
Situation similar to ARDS
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Forms of infection
Immunocompetent individuals:
asymptomatic seroconversion
Immunocompromised population:
intersticial pneumonia (if CD4 decreased bellow
200/ul): proliferation of organism with low or
no inflammatory responce
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Clinics
Fever
Non-productive mild cought
Dyspnoe; chest pain
Tachypnoe
Patients with prophylaxis: symptoms milder
BUT increased risk of dissemination;
increased risk of pneumothorax
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Clinics II
Auscultation: crackles; often normal
finding
Extrapulmonary (about 1% of cases):
Lymphadenopathy
Hepatosplenomegaly
Chorioid leasions
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Pneumocystis pneumonia
Foamy exsudate in the lungs affected by P. carinii; calcifications
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Diagnostics
Increased LDH: over 220 (non-specific)
Puls oxymetry: desaturation
Blood gases: hypoxemy, decreased CO2
RTG: intersticial pneumonia
High resolution CT
Bronchoscopy (associated with BAL)
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Imaging studies
RTG
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Imaging studies II
CT
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Diagnostics II
Direct detection of Pneumocystis:
parasitological examination:
Sputum: 30%
Induced sputum: 60%
Bronchoalveolar lavage: 90%
Microscopy vs PCR
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Pneumocystis jiroveci
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Therapy
Trimetoprim/sulfametoxazol
Trimetoprim 15-20 mg/kg/day
Sulfametoxazol 100 mg/kg/day in 6 doses
Pentamidine
4 mg/kg/day iv
Dapsone
100 mg/day po + trimetoprim 5 mg/kg/day
21 days
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Site of terminal multiplication
(not port of entry)
Paragonimus spp.
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Paragonimus spp.
Fluke; parasite of carnivores
Distribution: tropical and subtropical regions (Asia, Africa, and Latin America)
Prevalence of infection in endemic areas: 0.1-23.75%
8 species causing significant disease in human; most important
P. westermani
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Epidemiology
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Life cycle
2 intermediate hosts
specific fresh water snail
(Pleuroceridae, Thiaridae, Hydrobiidae,Semisulcospira libertina)
crustacean: crabs or crayfish (Geothelphusa, Sinopotamon, Parathelhusa, Cambaroides, Procambarus… )
+ human
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Life cycle
Egg
Miracidium
Redia
Metacerkaria
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Development in human host
Intestine abdominal wall/liver (1 week)
diaphragm lungs
Patent period: 5-6 weeks pi (eggs found in sputum
or in the stool)
Life expectacy of fluke: 20 years
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Experimental infection:
migration into pleural cavity
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Clinics
Incubation period: 2-20 days
20% of patients are asymptomatic
Acute phase: intestinenal phase
respiratory phase
Chronic phase: pulmonary vs
extrapulmonary symptoms
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Acute disease
Intestinal phase: abdominal pain, diarrhea
and urticaria
Lung phase: fever, cough, dyspnea, chest
pain, malaise, and sweats
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Chronic disease: pulmonary
6 months after infection
Often mistaken for tuberculosis
Dry cough followed by a cough productive of tenacious and rusty or golden sputum
Peripheral eosinophilia, increased temperature (no fever)
Hemoptysis
Vague chest discomfort, dyspnea on exertion, or wheezing
Wïthout treatment: fibrosis of lungs, cor pulmonale
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Pathology
Cyst of fluke in trachea Flukes in lungs (exp. inf. dog)
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Histopathology
Eggs in lung section
Adult fluke in lung section
Eggs within bronchi
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Chronic disease: extrapulmonary
Cerebral, abdominal, subcutaneous, and
miscellaneous
Either migration of adult fluke or eggs
entering the circulation being carried to
different organs
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Extrapulmonary disease
Cysts in the intestinal wall, liver, spleen, abdominal wall, peritoneal cavity, or mesenteric lymph nodes: bloody diarrhea or abdominal pain.
Cerebral form: mainly in children
(up to 1%): meningoencephalitis (headache, vomiting, seizures, or weakness, Jacksons epilepsy)
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Histopathology
Eggs of fluke, brain Calcified ova, brain
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Physical examination:
acute pulmonary disease
Clubbing of fingers
(hypoxemia)
Auscultation: signs of
pneumonia (crackles,
dullness to percussion)
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Physical examination:
chronic pulmonary disease
Similar to chronic bronchitis or
bronchiectasis
Profuse expectoration, pleuritic chest pain,
dyspnea, cough, occasional hemoptysis
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Physical examination:
extrapulmonary disease
Cerebral: palsy, hemiplegia, seizures, and paraplegia
Ocular: impaired visual acuity: optic atrophy, papilledema, and hemianopsia
Spinal: monoplegia, paraplegia, lower extremity paresthesias, or sensory loss
Abdominal: palpable masses
Kidneys: hematuria
Subcutaneous: migratory swelling or subcutaneous nodules containing immature flukes (often in lower abdominal and inguinal region)
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Laboratory studies
Eosinophilia (10-30%)
Total WBC: normal
Ova detected: in sputum, feaces, pleural
fluid, cerebrospinal fluid (CSF), or pus
Worms or eggs: biopsy of involved organ
Sputum detection: 50% (recommended
multiple examinations)
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Imaging studies
RTG: ring shadows, representing cavitating lesions, fibrosis, nodules or linear infiltrates with calcified foci, loculated pleural effusions, and pleural thickening
soap bubble sign of frontal lobes
CT/NMR: cerebral calcification, cystic lesions, or hydrocephalus
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RTG
Patchy infiltrate; cystic cavities Small pneumotorax due to migration
of flukes into the lungs
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CT; PET
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Involvement of the brain
Leasions within brain; hydrocephalus Soap bubble sign, RTG
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Diagnostics
Serology: complement fixation test, ELISA,
Immunoblot
Skin test: false positive results may occur,
epidemiological studies more than
diagnostics
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Diagnostics
CSF: numerous eosinophils
Thoracentesis: serosanguineous, has more than 1000 red cells with accompanying eosinophilia; low glucose
Lung biopsy: multiple worms or eggs
Adults found in cysts (mostly right lung): granulation tissue with fibroblasts, mononuclear cells, plasma cells, lymphoid cells, and eosinophils; Charcot-Leyden crystals
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Therapy
Praziquantel: 25 mg/kg PO tid for 2 d
Extrapulmonary lesions should be surgically
excised.
An intraventricular shunt may be needed to
manage hydrocephalus
Persistent seizures in cerebral involvement
Prognosis: good, with therapeutic cure rates
between 90 and 100%
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Site of possible terminal
multiplication (not port of entry)
Toxocara canis/cati
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Toxocara canis/cati
Roundworm
Distribution: worldwide
Eggs – the soil of parks and playgrounds
Transmission: per os
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Epidemiology
Epidemiology: 2-5% positive rate in urban
Western countries
14.2-37% in rural areas of Western countries
Tropical countries:
63.2% in Bali,
86% in Saint Lucia (West Indies), and
92.8% in La Reunion (French Overseas
Territories, Indian Ocean)
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Life cycle
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Disease in dog
5-51% positive dogs in Europe
Adult: 10 cm long
Similar to Ascaris infection in human
Ability to form „sleeping larvae“ –
transplacentary/transmammary transmission
Prepatent period: 56 days
Eggs shed to the environment are immature
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Maturation of eggs
Temperature + humidity
28-30°C – 15 days
Below 10°C – no maturation
Viability of the eggs in the outer environment:
5 years
If is the outer environment anaerobic – viability 6-8 months
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Human
Infectious agent: mature eggs; sleeping
larvae in the paratenic hosts
Accidental host; Paratenic host
Larvae: 0.02mm x 0.5mm
Zoonosis
Disease usually asymptomatic/mild
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Symptomatic disease
Number of the larvae in the host
Allergic reaction
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Pathophysiology
Migration of the larvae in the host:
- Allergic reaction (eosinophilic)
- Mechanic destruction of the tissue
- Proteolytic enzymes production by larvae
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Human
Larva migrans visceralis (liver, lung,
muscle and brain)
Larva migrans ocularis (eye)
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Anamnesis
Living with or raising dogs and cats
Eating without hand washing
Infection from contact with soil from a
yard, sandbox, park, or playground
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Larva migrans visceralis
Diarrhoea, abdominal pain, anorexia, nausea, fatigue
Pruritus, rash
Liver
Lungs: Cought, temperature (38°C), bronchospasm, wheezing
Brain: Difficulty sleeping, abdominal pain, headaches, and behavioral problems, seizures, temperature
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Examination
Hepatomegaly, splenomegaly
lymphadenitis, and wheezing
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Larva migrans visceralis: laboratory
Elevation of the leukocytes
Eosinophilia (20-90%)
Diagnostics: Serology (ELISA)
Biopsy
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Imaging studies
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Therapy
Dont treat positive titres if person
asymptomatic!!!!
Mebendazole (Vermox) - 25 mg/kg/d PO
single dose for 4 wk
Albendazole (Albenza) - 10 mg/kg/d PO
single dose for 4 wk
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Site of possible terminal
multiplication (not port of entry)
Echinococcus
granulosus/multilocularis
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Transitory site of development
Ascaris lumbricoides, Strongyloides stercoralis, Ancylostoma duodenale, Necator americanus,
Toxocara canis/cati, Schistosomiasis, Echinococcosis
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Life cycle of many parasites involves
specific developmental changes
taking place within lungs
Patient usually asymptomatic
(not in severe infection)
Affection of lung is transitory,
histopathological changes are
transitory
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Migration of parasites: eosinophilia
Lung phase: (pneumonia): damage of
cappillaries and alveoli -
cought, chest pain, subfebrilia
blood in the sputum
Sputum positive for detection of larvae of the
parasites (if examinated)
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Histopathology
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Imaging studies
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Symptoms lasting for particular time
After finish of development parasite
migrates to definitive pathological site
(intestine, portal venous system, …)
Therapy: specific (low detection);
corticosteroids