Paracoccidioidomycosis

Source: Wikipedia, the free encyclopedia.
Paracoccidioidomycosis
Other namesSouth American blastomycosis,
Antifungal medication[6]
MedicationItraconazole, amphotericin B,[6] trimethoprim/sulfamethoxazole[7]
Deaths200 deaths per year in Brazil[1]

Paracoccidioidomycosis (PCM), also known as South American blastomycosis, is a

fungal infection that can occur as a mouth and skin type, lymphangitic type, multi-organ involvement type (particularly lungs), or mixed type.[1][6] If there are mouth ulcers or skin lesions, the disease is likely to be widespread.[1] There may be no symptoms, or it may present with fever, sepsis, weight loss, large glands, or a large liver and spleen.[4][7]

The cause is fungi in the genus Paracoccidioides, including Paracoccidioides brasiliensis and Paracoccidioides lutzii,[8] acquired by breathing in fungal spores.[6]

Diagnosis is by sampling of

antifungals; itraconazole.[1][7] For severe disease, treatment is with amphotericin B followed by itraconazole, or trimethoprim/sulfamethoxazole as an alternative.[1][7]

It is endemic to Central and South America,[9] and is considered a type of neglected tropical disease.[8] In Brazil, the disease causes around 200 deaths per year.[1]

Signs and symptoms

Lesions due to Paracoccidioidomycosis on the face of a Brazilian child

Asymptomatic lung infection is common, with fewer than 5% of infected individuals developing clinical disease.[10]

It can occur as a mouth and skin type, lymphangitic type, multi-organ involvement type (particularly lungs), or mixed type.[1][6] If there are mouth ulcers or skin lesions, the disease is likely to be widespread.[1] There may be no symptoms, or it may present with fever, sepsis, weight loss, large glands, or a large liver and spleen.[4][7]

Two presentations are known, firstly the

chronic form, predominantly affecting adult men.[12] Most cases are infected before age 20, although symptoms may present many years later.[13]

Juvenile (acute/subacute) form

The juvenile, acute form is characterised by symptoms, such as fever, weight loss and

Adult (chronic) form

The chronic form presents months to years after the initial infection occurs and most frequently presents with dry cough and shortness of breath.

difficulties with voice control.[14] Upper respiratory tract mucosal lesions may be present, as well as increased mucus production and coughing up blood.[18] Both pulmonary and extrapulmonary involvement is common.[14]

Up to 70% of cases have mucosal involvement, with lesions often found in the mouth,

oropharynx, larynx, and palate. Classic lesions are superficial painful granular ulcers, with small spots of bleeding.[15]

Cause

Paracoccidioidomycosis is caused by two species of

fungi that can exist as a mold or yeast depending on temperature, P. brasiliensis and P. lutzii.[19] In protected soil environments, near water sources, that are disturbed either naturally or by human activity, P. brasiliensis has been epidemiologically observed (although not isolated).[20] A known animal carrier is the armadillo.[13] In the natural environment, the fungi are found as filamentous structures, and they develop infectious spores known as conidia.[13]

Human to human transmission has never been proven.[21]

Mechanism

Primary infection, although poorly understood due to lack of data, is thought to occur through inhalation of the

conidia through the respiratory tract, after inhaling fungal conidia produced by the mycelial form of P. brasiliensis.[14][21] This occurs predominantly in childhood and young adulthood, after exposure to agricultural activity.[13] Infection may occur through direct skin inoculation, although this is rare.[15]

After inhalation into the alveoli, there is rapid multiplication of the organism in the lung tissue, sometimes spreading via the venous and lymphatic systems.[14] Approximately 2% of people develop clinical features after the initial asymptomatic infection.[15]

The type of immune response determines the clinical manifestation of the infection, with children and

B lymphocytes, high levels of circulating antibodies, eosinophilia, and hypergammaglobulinemia.[13]

Lung involvement subsequently occurs after a dormant phase, manifesting in upper respiratory tract symptoms, and lung infiltrates on imaging.[15] The commonest, chronic form, is almost certainly a reactivation of the disease,[15] and may develop into progressive scarring of the lungs (pulmonary fibrosis).[22]

It can cause disease in those with normal immune function, although immunosuppression increases the aggressiveness of the fungus. It rarely causes disease in fertile-age women, probably due to a protective effect of estradiol.[23]

Diagnosis

More than 90% of cases can be diagnoses with direct

H&E) stain revealing large yeast cells with translucent cell walls with multiple buds.[14]

In the juvenile form, lung abnormalities are shown in high-resolution

CT scans of the lungs, whereas in the chronic form plain X-rays may show interstitial and alveolar infiltrates in the central and lower lung fields.[14]

Culture of P. brasiliensis takes between 20 and 30 days, requiring multiple samples and culture media. Initial culture can occur at room temperature, however after growth is noted, confirmation occurs by incubating at to 36-37 degrees to transform the fungus into yeast cells.[14]

H. capsulatum.[14]

Differential diagnosis

The disease can appear similar to

Treatment

Both P. brasiliensis and P. lutzii are

Co-trimoxazole is a second line agent, and is preferred for those with brain involvement, and during pregnancy.[13] For severe cases, intravenous treatment with amphotericin B is indicated, for an average of 2 to 4 weeks.[13]Prednisolone prescribed at the same time may reduce inflammation during treatment.[13] Patients should be treated until stabilisation of symptoms, and increase in body weight. Advice in regards to nutritional support, as well as smoking and alcohol intake should be provided. Adrenal insufficiency, if found, is treated with corticosteroids.[24] Clinical criteria for cure includes the absence or healing of lesions, stabilisation of body weight, negative as well as negative autoantibody tests.[13] There is insufficient data to support the benefits of above drugs to treat the disease.[25]

Epidemiology

Paracoccidioidomycosis is endemic in rural areas of Latin America, from southern Mexico to Argentina, and is also found in Brazil, Colombia, Venezuela, Ecuador and Paraguay.[13][15] An epidemic outbreak has never been observed.[13] It has the highest prevalence of all systemic mycoses (fungal infections) in the area.[12] As many as 75% of people in endemic areas have been estimated to be infected with the asymptomatic form (up to 10 million people), with 2% developing clinically significant disease.[12] Morbidity and mortality is strongly associated with patient's socioeconomic background,[12] with most adult patients being male agricultural workers.[26] Other risk factors include smoking, alcohol use, HIV co-infection or other immunosuppression.[21] 80% of reported cases are in Brazil, in the southeast, midwest, and south, spreading in the 1990s to the Amazon area. Most of the remaining infections are in Argentina, Colombia and Venezuela.[21] Most epidemiological reports have focused on P. brasliensis, with P. lutzii epidemiology poorly understood as of 2015.[21]

Rising cases have been linked to agriculturalization and deforestation in Brazil, urbanisation to peripheral city areas with poor infrastructure, as well as increased soil and air humidity.[13][21] One Brazilian indigenous tribe, the Surui, after changing from subsistence agriculture to coffee farming showed higher infection rates than surrounding tribes.[21]

There have also been reports in non-endemic areas with the rise of eco-tourism, in the United States, Europe and Japan.[15] All reported cases were returned travellers from endemic regions.[21]

History

Lutz-Splendore-de Almeida disease[3] is named for the physicians Adolfo Lutz,[27] Alfonso Splendor (1871–1953), an Italo-Brazilian parasitologist[28] and Floriano Paulo de Almeida (1898–1977), a Brazilian pathologist specializing in Pathologic Mycology (Study of Infectious Fungi),[29][30] who first characterized the disease in Brazil in the early 20th century.

See also

  • North American blastomycosis

References

  1. ^ .
  2. ^
    Who Named It?
  3. ^ a b c d e f g h i "ICD-11 - ICD-11 for Mortality and Morbidity Statistics". icd.who.int. Retrieved 26 June 2021.
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  20. OCLC 990065894.{{cite book}}: CS1 maint: location missing publisher (link
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  24. ^ Lutz A (1908), "Uma mycose pseudococcidioidica localizada no boca e observada no Brasil. Contribuicao ao conhecimento das hypoblastomycoses americanas.", Imprensa Médica (in Portuguese), 16, Rio de Janeiro: 151–163
  25. ^ Splendore A (1912), "Zimonematosi con localizzazione nella cavita della bocca osservata nel Brasile", Bulletin de la Société de pathologie exotique (in French), 5, Paris: 313–319
  26. ^ De Almeida FP (1928), "Lesoes cutaneas da blastomicose en cabaios experimentalmente infeetados", Anais da Faculdade de Medicina de Universidade de São Paulo (in Portuguese), 3: 59–64
  27. ^ de Almeida FP, da Silva Lacaz C (1942), "Micoses broco-pulmonares", Comp. Melhoramentos (in Portuguese), São Paulo: 98 pages

External links