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Lung Parasitic Infections

The document discusses Pneumocystis jiroveci (Pneumocystis carinii), a fungus-like microorganism that is the causative agent of pneumocystic pneumonia, primarily affecting immunocompromised individuals. It covers the organism's life cycle, epidemiology, clinical presentation, diagnosis, and treatment of pneumocystis pneumonia. The document also briefly mentions Paragonimus spp. and Toxocara canis/cati as other parasites that can infect the lungs.

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0% found this document useful (0 votes)
53 views71 pages

Lung Parasitic Infections

The document discusses Pneumocystis jiroveci (Pneumocystis carinii), a fungus-like microorganism that is the causative agent of pneumocystic pneumonia, primarily affecting immunocompromised individuals. It covers the organism's life cycle, epidemiology, clinical presentation, diagnosis, and treatment of pneumocystis pneumonia. The document also briefly mentions Paragonimus spp. and Toxocara canis/cati as other parasites that can infect the lungs.

Uploaded by

waheeda
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF, TXT or read online on Scribd
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Lung parasitic infections;

Pneumocystosis

Jarmila Kliescikova, MD
Respiratory system
Examination of the thorax

 Inspection (globally, locally)


 Percussion
 Auscultation
Laboratory examination

 Sputum
 Induced sputum
 BAL

 Pulmonary function examination


 Imaging studies
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)


Site of terminal multiplication
(port of entry)

Pneumocystis jiroveci
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…
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%
Life cycle
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
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
Pathophysiology

 Destruction of basal membrane leads to


changes in permeability of
alveoli/capillaries
 Changes in rate ventilation/perfusion
 Situation similar to ARDS
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
Clinics

 Fever
 Non-productive mild cought

 Dyspnoe; chest pain

 Tachypnoe

Patients with prophylaxis: symptoms milder


BUT increased risk of dissemination;
increased risk of pneumothorax
Clinics II

 Auscultation: crackles; often normal


finding
 Extrapulmonary (about 1% of cases):
Lymphadenopathy
Hepatosplenomegaly
Chorioid leasions
Pneumocystis pneumonia

Foamy exsudate in the lungs affected by P. carinii;


calcifications
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)
Imaging studies

RTG
Imaging studies II

CT
Diagnostics II

 Direct detection of Pneumocystis:


parasitological examination:
Sputum: 30%
Induced sputum: 60%
Bronchoalveolar lavage: 90%
 Microscopy vs PCR
Pneumocystis jiroveci
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
Site of terminal multiplication
(not port of entry)

Paragonimus spp.
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
Epidemiology
Life cycle
2 intermediate hosts
 specific fresh water snail
(Pleuroceridae, Thiaridae,
Hydrobiidae,Semisulcospira
libertina)
 crustacean: crabs or crayfish
(Geothelphusa, Sinopotamon,
Parathelhusa, Cambaroides,
Procambarus… )
+ human
Life cycle
Egg

Miracidium

Redia

Metacerkaria
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


Experimental infection:
migration into pleural cavity
Clinics
 Incubation period: 2-20 days
 20% of patients are asymptomatic
 Acute phase: intestinenal phase
respiratory phase
 Chronic phase: pulmonary vs
extrapulmonary symptoms
Acute disease

 Intestinal phase: abdominal pain, diarrhea


and urticaria

 Lung phase: fever, cough, dyspnea, chest


pain, malaise, and sweats
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
Pathology
Cyst of fluke in trachea Flukes in lungs (exp. inf. dog)
Histopathology

Eggs in lung section

Adult fluke in lung section

Eggs within bronchi


Chronic disease: extrapulmonary

 Cerebral, abdominal, subcutaneous, and


miscellaneous

 Either migration of adult fluke or eggs


entering the circulation being carried to
different organs
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)
Histopathology

Eggs of fluke, brain Calcified ova, brain


Physical examination:
acute pulmonary disease

 Clubbing of fingers
(hypoxemia)
 Auscultation: signs of
pneumonia (crackles,
dullness to percussion)
Physical examination:
chronic pulmonary disease

 Similar to chronic bronchitis or


bronchiectasis
 Profuse expectoration, pleuritic chest pain,
dyspnea, cough, occasional hemoptysis
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)
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)
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
RTG

Patchy infiltrate; cystic cavities Small pneumotorax due to migration


of flukes into the lungs
CT; PET
Involvement of the brain

Leasions within brain; hydrocephalus Soap bubble sign, RTG


Diagnostics

 Serology: complement fixation test, ELISA,


Immunoblot
 Skin test: false positive results may occur,
epidemiological studies more than
diagnostics
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
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%
Site of possible terminal
multiplication (not port of entry)

Toxocara canis/cati
Toxocara canis/cati

 Roundworm
 Distribution: worldwide
 Eggs – the soil of parks and playgrounds
 Transmission: per os
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)
Life cycle
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
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
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
Symptomatic disease

 Number of the larvae in the host


 Allergic reaction
Pathophysiology

 Migration of the larvae in the host:


- Allergic reaction (eosinophilic)
- Mechanic destruction of the tissue
- Proteolytic enzymes production by larvae
Human

 Larva migrans visceralis (liver, lung,


muscle and brain)

 Larva migrans ocularis (eye)


Anamnesis

 Living with or raising dogs and cats


 Eating without hand washing
 Infection from contact with soil from a
yard, sandbox, park, or playground
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
Examination

 Hepatomegaly, splenomegaly
lymphadenitis, and wheezing
Larva migrans visceralis: laboratory

 Elevation of the leukocytes


 Eosinophilia (20-90%)

 Diagnostics: Serology (ELISA)


Biopsy
Imaging studies
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
Site of possible terminal
multiplication (not port of entry)

Echinococcus
granulosus/multilocularis
Transitory site of development

Ascaris lumbricoides, Strongyloides stercoralis,


Ancylostoma duodenale, Necator americanus,
Toxocara canis/cati, Schistosomiasis,
Echinococcosis
 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
 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)
Histopathology
Imaging studies
 Symptoms lasting for particular time
 After finish of development parasite
migrates to definitive pathological site
(intestine, portal venous system, …)
 Therapy: specific (low detection);
corticosteroids

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