Pulmonary thromboembolism as a rare complication of Plasmodium vivax malaria: A case report.

Key Clinical Message: Low threshold is required to suspect complications of Plasmodium vivax malaria. Pulmonary thromboembolism, though rare, should be considered as its complication in the presence of unexplained and sudden onset shortness of breath. Abstract: The hypercoagulable complications of malaria typically manifest in the microvasculature. However, there are several cases of intracranial venous thrombosis caused by Plasmodium falciparum and Plasmodium vivax malaria, and there was one case report of pulmonary thromboembolism (PTE) due to P. falciparum. A 30-year-old Ethiopian male patient presented with sudden onset of shortness of breath for 3 days. He had also high-grade fever, chills, and rigors associated with loss of appetite and fatigue of similar duration. He was from malaria endemic area. He had a pulse rate of 108 beats per minutes, respiratory rate of 32 breaths per minute, oxygen saturation of 82% with atmospheric air and temperature of 38.9°C. Further examination revealed accentuation of pulmonary component of second heart sound. Complete blood count revealed mild anemia and peripheral blood film showed trophozoites of P. vivax. Pulmonary CT angiography showed filling defects in the right and left pulmonary arteries. The patient was diagnosed to have P. vivax malaria complicated by PTE. He was managed with intranasal oxygen, antimalarial agent, and anticoagulation. Upon serial evaluations on the third week and second month of follow up, he did not have complaints and physical examination was non-remarkable. Malaria is a protozoan disease with high mortality and morbidity. For a long time, severe cases of malaria were thought to be mostly caused by P. falciparum. However, recent evidences have shown a paradigm shift and we should remember that P. vivax can also cause severe malaria and this can be complicated by hypercoagulable conditions including PTE.

Polyserositis caused by tuberculosis in a young female patient with hypothyroidism: A diagnostic challenge.

Key Clinical Messages: The diagnosis of polyserositis due to tuberculosis (TB) is complex and challenging, which may cause delays in treatment. TB should be ruled out first before attributing polyserositis to any other cause like hypothyroidism, particularly in high TB burden countries. Abstract: Polyserositis has numerous causes and frequently occurs in neoplasia, autoimmune disorders, endocrine conditions like hypothyroidism, and infectious diseases like tuberculosis (TB). The diagnosis of TB polyserositis is complex and challenging, which may cause the start of definitive therapy to be delayed. Here, we report the case of a 32-year-old female patient who presented with abdominal distension for 3 weeks associated with shortness of breath, cough, excessive fatigue, and loss of appetite. Thyroid function tests were suggestive of primary hypothyroidism, and later on, sputum GeneXpert MTB/RIF test turned out to be positive. She was initially started on oral levothyroxine and then anti-TB medications. The polyserositis resolved a month after the initiation of anti-TB drugs. TB should be ruled out first before attributing polyserositis to any other cause like hypothyroidism, particularly in high TB burden countries. Microbiologic tests, such as GeneXpert, remain the most important tools to make a diagnosis of TB and start anti-TB medications early.

Budd-Chiari Syndrome as an Initial Presentation of Systemic Lupus Erythematosus Associated with Antiphospholipid Syndrome: A Case Report with Review of the Literature.

Introduction: Budd-Chiari syndrome (BCS) is a rare disorder characterized by hepatic outflow obstruction. It can be classified as primary or secondary BCS. Common causes of BCS include myeloproliferative diseases, infections, malignancies, and systemic autoimmune illnesses. Systemic lupus erythematosus (SLE) can be complicated with BCS. However, only a few case reports have described the uncommon occurrence of BCS as a primary presentation of SLE. Case Presentation: We report the case of a 32-year-old female patient who presented with progressive abdominal distension of four months. On the abdominal CT scan, the left and middle hepatic veins were not visualized; the right hepatic vein and intrahepatic IVC had luminal narrowing; and there was caudate lobe enlargement suggestive of Budd-Chiari syndrome (BCS). Six months after the diagnosis of BCS, the patient developed other clinical features suggestive of systemic lupus erythematosus (SLE) and was finally diagnosed with SLE. Conclusion: Acquired or inherited thrombotic conditions are the most common underlying causes of Budd-Chiari syndrome. Systemic lupus erythematosus (SLE) is the most common cause of secondary APS and most patients present with Budd-Chiari syndrome as a manifestation of APS after the diagnosis of SLE. In rare cases, such as the current case, Budd-Chiari syndrome can present even before the diagnosis of SLE. Hence, we would like to emphasize that Budd-Chiari syndrome can be an initial presentation of SLE.

Tissue (re)distribution of Trypanosoma equiperdum in venereal infected and blood transfused horses.

Dourine, caused by Trypanosoma equiperdum, is a life-threatening venereal disease in equidae. So far, there is no clear evidence on how and when stallions become infectious, nor which tissues are affected by the parasite in diseased animals. Post-infection, after a transient, temporary phase of parasitaemia, the parasite disperses to different tissues in an unknown distribution pattern. This study describes the distribution of the parasite after infection by artificial insemination (AI) or blood transfusion. Mares (N = 4) were artificially inseminated with T. equiperdum spiked semen whereas stallions (N = 4) were infected by blood transfusion. The course of the disease was monitored by parasitological (Woo) and molecular (PCR) tests and clinical signs and haematological parameters were recorded. At 120 days post infection, horses had a full necropsy, histopathology and PCR. A similar pattern of parasitaemia, disease progression and tissue distribution were seen in all horses. Ejaculated semen in the preclinical stage and epididymal semen in the chronic stage of the disease was positive on PCR and caused infection in mice. Cymelarsan® treatment in the chronic stage did not result in a clinico-haematological or histopathological improvement. At necropsy, lesions were observed in the nervous and reproductive system. Histopathological lesions were most severe in the peripheral nerves and associated ganglia, the testicles and genital mucosae with multifocal infiltration of lymphocytes, plasma cells and histocytes. The parasites disseminated to several tissues including the nervous system, testicles and semen. The results indicate that transmission of T. equiperdum is possible through semen even from symptomless stallions post-treatment.