DOCSLIB.ORG

Complete Recovery from Cryptosporidium Parvum Infection

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Complete Recovery from Cryptosporidium Parvum Infection Bone Marrow Transplantation (2003) 32, 733–737 & 2003 Nature Publishing Group All rights reserved 0268-3369/03 $25.00 www.nature.com/bmt Case Report Complete recovery from Cryptosporidium parvum infection with gastroenteritis and sclerosing cholangitis after successful bone marrow transplantation in two brothers with X-linked hyper-IgM syndrome S Dimicoli1, D Bensoussan1, V Latger-Cannard2, J Straczek3, L Antunes4, L Mainard5, A Dao6, F Barbe3, C Araujo7, L Cle´ ment7, P Feugier7, T Lecompte2, JF Stoltz1 and P Bordigoni7 1Unite´ de The´rapie Cellulaire et Tissus, CHU de Nancy, Alle´e du Morvan, 54511 Vandoeuvre les Nancy, France; 2Laboratoire d’He´matologie Biologique, CHU de Nancy, Alle´e du Morvan, 54511 Vandoeuvre les Nancy, France; 3Laboratoire de Biochimie, CHU de Nancy, Alle´e du Morvan, 54511 Vandoeuvre les Nancy, France; 4Laboratoire d’Anatomo-Pathologie, CHU de Nancy, Alle´edu Morvan, 54511 Vandoeuvre les Nancy, France; 5Service de Radiologie Pe´diatrique, CHU de Nancy, Alle´e du Morvan, 54511 Vandoeuvre les Nancy, France; 6Laboratoire de Parasitologie et Mycologie CHU de Nancy, Alle´e du Morvan, 54511 Vandoeuvre les Nancy, France; 7Service de Me´decine infantile 2, CHU de Nancy, Alle´e du Morvan, 54511 Vandoeuvre les Nancy, France Summary: parvum, Histoplasmosa capsulata and Leishmania. Dysimmunity and malignancy are classical complica- We describe two brothers who suffered from hyper-IgM tions.1,2 syndrome (HIGM1) with similar clinical features: recur- CD40L, a membrane glycoprotein, is transiently ex- rent infections, especially cryptosporidium gastroenteritis pressed on activated CD4 þ and CD8 þ T cells, mast cells, with cholangitis. Their activated T cells did not express basophils, eosinophils and platelets. CD40, the CD40L CD40L. Nucleotide sequencing revealed a mutation in receptor, is a member of the TNF receptor family found on both boys with respect to intron 4 and exon 5 boundaries B cells, monocytes, dendritic cells, epithelial cells, fibro- of the CD40L gene in Xq26. They underwent successful blasts and some malignant cells. CD40 expression can also bone marrow transplantation (BMT) from HLA-geno- be induced on different cells by gamma interferon (IFNg).3,4 identical siblings. The Cryptosporidium infection and Thus, a potential mechanism contributing to C. parvum cholangitis resolved thereafter. At 6 months after BMT, immunity could be a direct triggering of apoptosis in expression of CD40L on activated T lymphocytes was CD40 þ infected cells by CD40L expressed on activated normal. After 1 year, both boys are well, and immune T cells. More recently, Hayward et al 4 have shown in a reconstitution has improved. Based on these two successful mouse model that CD40 expression on intestinal epithelial experiences, BMT with a genoidentical sibling seems a cells is not required for C. parvum clearance. Moreover, C. reasonable therapeutic approach for HIGM1, if Crypto- parvum infection can be cleared only when CD40 is present sporidium infection occurs. on dendritic and mononuclear phagocyte cells. Interleukin Bone Marrow Transplantation (2003) 32, 733–737. 12 production by these antigen-presenting cells leads doi:10.1038/sj.bmt.1704211 activated T cells (via CD40-CD40L pathway) to produce Keywords: X-linked immunodeficiency with hyper-IgM; TH1 cytokines such as IFNg. CD40 Ligand; cryptosporidum parvum gastroenteritis; C. parvum, a coccidian parasite, infects the intestine sclerosing cholangitis and sometimes the respiratory tract. In immunocompro- mised patients, it may cause severe intestinal fluid loss, with dehydration, chronic diarrhea and malnutrition. Hyper-IgM Syndrome (HIGM1) is a primary immuno- Several antimicrobial treatments have been tried but deficiency associated with mutations in the gene encoding none has proven effective. As previously reported by 5 the CD40L, located at Xq26. Patients suffer recurrent Hayward et al, patients with HIGM1 are at increased sinopulmonary and gastrointestinal infections, opportunis- risk of cholangiopathy, especially with C. parvum tic infections due to Pneumocystis carinii, Cryptosporidium infection. Curative therapy of HIGM1 relies on bone marrow transplantation (BMT), from an HLA-matched sibling, as first reported by Thomas et al,6,7 or from matched unrelated donors.8 However, the presence of C. parvum Correspondence: Dr D Bensoussan, Unite de Therapie´ Cellulaire et infection, especially when complicated by sclerosing cho- tissus, CHU de Nancy, Alle´ e du Morvan, 54511 Vandoeuvre-Les-Nancy. langitis, impairs the results of BMT. Khawaja et al 9 E-mail: [email protected] The first two authors contributed equally to this work reported three cases where patients suffering from severe Received 6 November 2002; accepted 8 April 2003 C. parvum infection died soon after BMT.9 BMT for HIGM1 and Cryptosporidium infection S Dimicoli et al 734 In this report, we describe two brothers with HIGM1 who were both suffering from severe C. parvum infection with gastroenteritis and sclerosing cholangitis. They under- went successful BMT from a genoidentical HLA sibling and recovered from the C. parvum infection. Materials and methods Case report Two brothers, had a family history of immune deficiency: two cousins suffered from HIGM1, one of whom died of diffuse C. parvum infection despite an HLA-sibling allogeneic bone marrow transplant together with an orthotopic liver transplant. Thanks to family screening, the two brothers were diagnosed with HIGM1, confirmed by the absence of CD40L expression on activated T lymphocytes. Sequencing of PCR-amplified CD40L genomic DNA revealed the Figure 1 Sclerosing cholangitis due to Cryptosporidium infection. A large bile duct is surrounded by a cuff of oedematous, inflamed fibrous tissue same mutation for the two brothers: a 10-nucleotide with an onion-skin appearance (arrow). Unaffected interlobular portal deletion (gTGTTACAGT) and a dinucleotide insertion tract (arrow head). Needle biopsy, H&E. (aa) at the intron 4/exon5boundary. This mutation predicts a premature termination of translation and generation of a truncated protein. The brothers presented similar clinical features. Treatment was initiated with intravenous (i.v.) serum aspartate and alanine amino transferase levels were immunoglobulin and P. carinii prophylaxis. five times above normal. Neutropenia and eosinophilia At 6 years of age, brother A had Cryptosporidium were also present. gastroenteritis with sclerosing cholangitis resulting in After considering the poor prognosis of this disease, persistent diarrhea and severe weight loss requiring especially when it is complicated by Cryptosporidium continuous enteral nutrition. The sclerosing cholangitis infection, and given the family history, the parents gave worsened and at MR-cholangiography, dilated extra and informed consent for their two sons to undergo BMT. The intrahepatic bile ducts were observed. Needle liver biopsy donors were two different HLA-identical sisters. revealed sclerosing cholangitis with prominent peri-portal The boys were conditioned with busulfan (4 mg/kg body concentric fibrosis, eosinophilic infiltration but no biliary weight per day for 4 days) followed by cyclophosphamide cirrhosis (Figure 1). Liver function tests were abnormal (50 mg/kg body weight per day for 4 days). Graft-versus- (Table 1). Alkaline phosphatase was elevated and serum host disease (GVHD) prophylaxis consisted of short-term aspartate and alanine amino transferase were six times methotrexate (15mg/m 2 on day 1 and 10 mg/m2 on days 3, above normal. There was also chronic, but not severe, 6, 11 after BMT), and cyclosporine A (3 mg/kg/day as a neutropenia and eosinophilia. continuous i.v. infusion on days À1to þ 30 and 6.25mg/kg Brother B had recurrent common sinus infections. At the twice daily from days 31 to 180 post-BMT). Infection age of 8 years, he also suffered from a Cryptosporidium prophylaxis included isolation in a laminar air-flow unit, infection with cholangiopathy, requiring enteral nutrition. oral administration of nonabsorbable antibiotics and The results of MR-cholangiography were similar to those treatment with i.v. immunoglobulins for 1 year (200 mg/ of A (Figure 2). Needle liver biopsy revealed cholangitis kg weekly for 3 months and then 400 mg/kg per month). with mild, nonconcentric, fibrotic enlargement of the portal The boys continued with enteral nutrition and anti- tracts and eosinophilic infiltration. Liver function tests were Cryptosporidium treatment (paromomycin 500 mg/day and also abnormal. Alkaline phosphatase was elevated and azithromycin 500 mg/day). Table 1 Liver function tests (patient A) Before C. Before BMT Day of BMT Day +15 post BMT Day +30 post BMT Day +60 post BMT Normal values parvum infection ALP 423 962 397 893 586 279 70–260 UI/l Total bilirubin 2 2 2 18 8 2 2–11 mg/l Direct bilirubin 1 1 1 9 2 1 o5 mg/l ALT 31 17546 12 8 12 5–40 UI/l AST 16 99 72 31 31 26 5–35 UI/l 50-nucleotidase 3 40 7 44 26 6 0–9 UI/l LDH 356 595 534 739 801 695 210–400 UI/l ALP: alkaline phosphatase, ALT: alanine amino transferase, AST: aspartate amino transferase. Bone Marrow Transplantation BMT for HIGM1 and Cryptosporidium infection S Dimicoli et al 735 Results Clinical course after BMT The clinical course for A was uneventful. At day 17, his absolute neutrophil count was over 500 per cubic millimeter and platelet counts were self-sustaining at levels above 50 000/ml at day 26. Neither GVHD nor veno-occlusive disease was observed. He had suffered from sinusitis (no organism identified) successfully treated by i.v. antibiother- apy. The Cryptosporidium infection disappeared soon after engraftment and was undetectable after day 60, despite immunological defects due to the allograft procedure. At 4 months after BMT, MR-cholangiography was significantly improved. After 19 months, stabilization of the cholangitis and decreased dilation of the extra and intrahepatic bile ducts was confirmed (Figure 2). Liver function tests normalized by day 60 post-BMT (Table 1). On day 200 post BMT, the quantitative and qualitative expression of CD40L on T cells was normal. DNA analysis revealed that 100% of lymphocytes and polynuclear cells were of donor origin.
Load more

Recommended publications
  • Campylobacter:What You Need to Know
    Queensland Health Campylobacter: what you need to know Campylobacter is one of the most Age groups most at risk common causes of foodborne illness Under in Australia. 60+ You can’t see it, smell it or even taste it on food, but if 5s it affects you, you won’t forget it. What is Campylobacter? Campylobacter is a little known foodborne bacteria similar to Salmonella. * In some cases Campylobacter can also lead to irritable 230,000 bowel syndrome, reactive arthritis and in rare cases cases a year Guillain-Barré syndrome—a type of paralysis. How do you get it? Most cases of Campylobacter infection are associated ** with eating raw or undercooked poultry or by cross 3200 contamination. hospitalisations as It is important to keep raw poultry and their juices a result of foodborne away from any already cooked or ready-to-eat foods illness caused by and fresh produce. Campylobacter Who is at risk? Anyone can be affected by Campylobacter but certain $1.25 billion people are at a greater risk for severe illness including annual total cost to society young children (under 5 years), older adults (over 60 for foodborne illness in years) and people with weakened immunity. Australia How to prevent it The easiest way to protect yourself and your family is to follow our four food safety tips every time you prepare raw poultry. ! Symptoms of Campylobacter Campylobacter infections cause gastroenteritis Follow these four safety tips (commonly known as gastro) diarrhoea, abdominal pains, cramping and fever. to prevent foodborne illness Symptoms usually start two to five days after from Campylobacter infection, and can last for one to three weeks.
    [Show full text]
  • Astroviruses As Causative Agents of Gastroenteritis
    Under the Microscope Astroviruses as causative agents of gastroenteritis with other enteric pathogens, especially rotaviruses, are known. Most infections in adults are asymptomatic. In other mammalian species, infection results in diarrhoea and gastroenteritis, while infection in birds leads to extraintestinal diseases, including Enzo A Palombo interstitial nephritis in young chicks and acute hepatitis in Environment and Biotechnology ducklings2. Centre Faculty of Life and Social Sciences Swinburne University of Epidemiology Technology Hawthorn VIC 3122 The first description of astrovirus came in 1975 after electron microscopic analysis of diarrhoeal stool samples from infants3,4. Astroviruses were first identified over 30 years ago and The unusual appearance of the virion particles (10% show a the virus was soon established as an important cause of characteristic five- or six-pointed star pattern on their surface) gastroenteritis, particularly in young children. Human indicated a previously unrecognised virus. Astroviruses have astrovirus disease was thought to result from infection since been reported worldwide in samples from infants and by a limited number of serotypes. However, recent young children with gastroenteritis. Soon after the first report in studies have indicated that the extent of genetic diversity humans, astrovirus-like particles were observed in domesticated is greater than previously assumed. In addition, the animals. There is now abundant evidence that astroviruses are widespread occurrence among animals and reports of widespread among domestic, synanthropic and wild animals, avian recombination and possible cross-species transmission and mammalian species in terrestrial and aquatic environments1. suggest that astroviruses have zoonotic potential. The list of animal species from which astroviruses have been Astroviruses are small (28–30 nm), non-enveloped viruses identified (chronologically) includes sheep, cattle, chickens, belonging to the family Astroviridae.
    [Show full text]
  • Evaluation of Abnormal Liver Chemistries
    ACG Clinical Guideline: Evaluation of Abnormal Liver Chemistries Paul Y. Kwo, MD, FACG, FAASLD1, Stanley M. Cohen, MD, FACG, FAASLD2, and Joseph K. Lim, MD, FACG, FAASLD3 1Division of Gastroenterology/Hepatology, Department of Medicine, Stanford University School of Medicine, Palo Alto, California, USA; 2Digestive Health Institute, University Hospitals Cleveland Medical Center and Division of Gastroenterology and Liver Disease, Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA; 3Yale Viral Hepatitis Program, Yale University School of Medicine, New Haven, Connecticut, USA. Am J Gastroenterol 2017; 112:18–35; doi:10.1038/ajg.2016.517; published online 20 December 2016 Abstract Clinicians are required to assess abnormal liver chemistries on a daily basis. The most common liver chemistries ordered are serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase and bilirubin. These tests should be termed liver chemistries or liver tests. Hepatocellular injury is defined as disproportionate elevation of AST and ALT levels compared with alkaline phosphatase levels. Cholestatic injury is defined as disproportionate elevation of alkaline phosphatase level as compared with AST and ALT levels. The majority of bilirubin circulates as unconjugated bilirubin and an elevated conjugated bilirubin implies hepatocellular disease or cholestasis. Multiple studies have demonstrated that the presence of an elevated ALT has been associated with increased liver-related mortality. A true healthy normal ALT level ranges from 29 to 33 IU/l for males, 19 to 25 IU/l for females and levels above this should be assessed. The degree of elevation of ALT and or AST in the clinical setting helps guide the evaluation.
    [Show full text]
  • Acute Pancreatitis Associated with Rotavirus Infection and Review Of
    Case Report/Olgu Sunumu İstanbul Med J 2020; 21(1): 78-81 DO I: 10.4274/imj.galenos.2020.88319 Acute Pancreatitis Associated with Rotavirus Infection and Review of The Literature Rotavirüs Enfeksiyonuna Bağlı Akut Pankreatit Olguları ve Literatürün Gözden Geçirilmesi Kamil Şahin, Güzide Doğan University of Health Sciences, Haseki Training and Research Hospital, Department of Pediatrics, İstanbul, Turkey ABSTRACT ÖZ Agents causing acute gastroenteritis are not common causes of Çocuklarda pankreatit etiyolojisinde akut gastroenterit etkenleri pancreatitis etiology in children. Pancreatitis associated with sık görülen sebeplerden değildir. Rotavirüs enfeksiyonuna rotavirus infection is very rare. Cases with acute pancreatitis bağlı görülen pankreatit ise oldukça nadirdir. Rotavirüs during rotavirus gastroenteritis are reported due to rare gastroenteriti sırasında akut pankreatit gelişen olgular, associations. In this article, the causes of acute pancreatitis rotavirüs enfeksiyonuna bağlı akut pankreatitin nadir olması and cases of acute pancreatitis due to rotavirus infection were nedeniyle sunulmuştur. Bu yazıda, akut pankreatit sebepleri ve investigated. Clinical findings were mild, and complications rotavirüse bağlı gelişen akut pankreatit olguları incelenmiştir. were not observed in both of our patients, including a two- İki yaş kız ve üç yaşındaki erkek iki olgumuzda ve literatürde year-old female and a three-year-old male, and other cases değerlendirilen diğer olgularda klinik bulgular hafif seyretmiş, evaluated in the literature. The
    [Show full text]
  • Hepatitis C – Screening, Diagnosis, Management & Treatment
    12 Osteopathic Family Physician (2019) 12 - 19 Osteopathic Family Physician | Volume 11, No. 1 | January/February, 2019 Review ARTICLE Hepatitis C – Screening, Diagnosis, Management & Treatment Michael Ferraro, DO & Matthew StantsPainter, DO Washington Health System Family Medicine Residency Program, Washington, PA KEYWORDS: Abstract: Hepatitis C virus (HCV) infection is a major cause of chronic liver disease, hepatocellular carcinoma and cirrhosis with at least 185 million people infected worldwide, causing 399,000 deaths Disease Prevention annually. HCV is transmitted through blood or body fluids. Transmission most commonly occurs and Wellness through sharing of injection drug, occupational exposure through needlestick injuries in healthcare Hepatitis C settings, and birth to an HCV infected mother. There are seven known genotypes of HCV, 1a, 1b, 2, 3, 4, 5, and 6, with the most common genotypes in the U.S. being 1a, 1b, 2, and 3, which comprise Infectious Disease approximately 97% of all U.S. HCV infections. Risks for disease progression include baseline liver histology, age, ethnicity, gender, alcohol use, comorbidities and immune response. There are Jaundice multiple screening recommendations currently in place, some of which are based on risk factors, Transaminitis with others based on legislation. The screening test of choice is the anti-Hepatitis C virus antibody, with a confirmatory HCV RNA PCR with genotyping. Once the diagnosis is made, assessing the level of fibrosis and/or cirrhosis is an important step in determining the pathway to treatment. There are multiple new options for treatment with improved efficacy and less side effects. Patient being treated for HCV should be monitored and assessed for compliance with therapy and adverse effects, including new or worsening psychiatric illness and screened for alcohol and substance abuse.
    [Show full text]
  • Acute Gastroenteritis
    Article gastrointestinal disorders Acute Gastroenteritis Deise Granado-Villar, MD, Educational Gap MPH,* Beatriz Cunill-De Sautu, MD,† Andrea In managing acute diarrhea in children, clinicians need to be aware that management Granados, MDx based on “bowel rest” is outdated, and instead reinstitution of an appropriate diet has been associated with decreased stool volume and duration of diarrhea. In general, drug therapy is not indicated in managing diarrhea in children, although zinc supplementation Author Disclosure and probiotic use show promise. Drs Granado-Villar, Cunill-De Sautu, and Objectives After reading this article, readers should be able to: Granados have disclosed no financial 1. Recognize the electrolyte changes associated with isotonic dehydration. relationships relevant 2. Effectively manage a child who has isotonic dehydration. to this article. This 3. Understand the importance of early feedings on the nutritional status of a child who commentary does has gastroenteritis. contain a discussion of 4. Fully understand that antidiarrheal agents are not indicated nor recommended in the an unapproved/ treatment of acute gastroenteritis in children. investigative use of 5. Recognize the role of vomiting in the clinical presentation of acute gastroenteritis. a commercial product/ device. Introduction Acute gastroenteritis is an extremely common illness among infants and children world- wide. According to the Centers for Disease Control and Prevention (CDC), acute diarrhea among children in the United States accounts for more than 1.5 million outpatient visits, 200,000 hospitalizations, and approximately 300 deaths per year. In developing countries, diarrhea is a common cause of mortality among children younger than age 5 years, with an estimated 2 million deaths each year.
    [Show full text]
  • A Drug-Induced Cholestatic Pattern
    Review articles Hepatotoxicity: A Drug-Induced Cholestatic Pattern Laura Morales M.,1 Natalia Vélez L.,1 Octavio Germán Muñoz M., MD.2 1 Medical Student in the Faculty of Medicine and Abstract the Gastrohepatology Group at the Universidad de Antioquia in Medellín, Colombia Although drug induced liver disease is a rare condition, it explains 40% to 50% of all cases of acute liver 2 Internist and Hepatologist at the Hospital Pablo failure. In 20% to 40% of the cases, the pattern is cholestatic and is caused by inhibition of the transporters Tobon Uribe and in the Gastrohepatology Group at that regulate bile synthesis. This reduction in activity is directly or indirectly mediated by drugs and their me- the Universidad de Antioquia in Medellín, Colombia tabolites and/or by genetic polymorphisms and other risk factors of the patient. Its manifestations range from ......................................... biochemical alterations in the absence of symptoms to acute liver failure and chronic liver damage. Received: 30-01-15 Although there is no absolute test or marker for diagnosis of this disease, scales and algorithms have Accepted: 26-01-16 been developed to assess the likelihood of cholestatic drug induced liver disease. Other types of evidence are not routinely used because of their complexity and cost. Diagnosis is primarily based on exclusion using circumstantial evidence. Cholestatic drug induced liver disease has better overall survival rates than other patters, but there are higher risks of developing chronic liver disease. In most cases, the patient’s condition improves when the drug responsible for the damage is removed. Hemodialysis and transplantation should be considered only for selected cases.
    [Show full text]
  • Stomach Flu (Viral Gastroenteritis)
    Stomach Flu (Viral Gastroenteritis) The stomach flu (also called viral gastroenteritis) is caused by a virus (rotavirus, adenovirus, Norwalk virus to name a few) that affect the stomach and small intestines. It may come on suddenly or over the course of a few hours. The illness is usually brief, lasting 24-72 hours. Symptoms include: Nausea Vomiting Stomach cramps Diarrhea Mild fever Fatigue Body Chills/Sweats Loss of appetite Muscle aches To help take care of yourself: • The best thing to do is to let your stomach rest from solid foods. • Sip on clear liquids (Hi-C, apple, cranberry, and grape juices, Jell-O, Gatorade- type liquids and ginger-ale or ginger tea). There are special properties in ginger that help soothe the stomach. It is extremely important to keep up your hydration. Water is great for hydration but Gatorade-type products are better because they will restore your electrolytes (Sodium, Potassium and Chloride) which are essential for body functions. You may "stir" the bubbles out of the soda if the carbonation is harsh on your stomach. • Once you have not vomited for a few hours and your stomach is feeling better, you may start to eat solid foods. You may try crackers, plain noodles, eggs, broth, pretzels and yogurt. • The BRAT diet (Bananas, Rice, Applesauce & Toast) includes foods that are low in fiber and are easily digested. • Stay away from dairy products, citric (including orange and grapefruit juices), tomato-based & spicy foods. • SLOWLY increase your dietary intake to include fruits, vegetables and meat once symptoms are gone (usually over 2-3 days).
    [Show full text]
  • Acute Liver Failure J G O’Grady
    148 Postgrad Med J: first published as 10.1136/pgmj.2004.026005 on 4 March 2005. Downloaded from REVIEW Acute liver failure J G O’Grady ............................................................................................................................... Postgrad Med J 2005;81:148–154. doi: 10.1136/pgmj.2004.026005 Acute liver failure is a complex multisystemic illness that account for most cases, but a significant number of patients have no definable cause and are evolves quickly after a catastrophic insult to the liver classified as seronegative or of being of indeter- leading to the development of encephalopathy. The minate aetiology. Paracetamol is the commonest underlying aetiology and the pace of progression strongly cause in the UK and USA.2 Idiosyncratic reac- tions comprise another important group. influence the clinical course. The commonest causes are paracetamol, idiosyncratic drug reactions, hepatitis B, and Viral seronegative hepatitis. The optimal care is multidisciplinary ALF is an uncommon complication of viral and up to half of the cases receive liver transplants, with hepatitis, occurring in 0.2%–4% of cases depend- ing on the underlying aetiology.3 The risk is survival rates around 75%–90%. Artificial liver support lowest with hepatitis A, but it increases with the devices remain unproven in efficacy in acute liver failure. age at time of exposure. Hepatitis B can be associated with ALF through a number of ........................................................................... scenarios (table 2). The commonest are de novo infection and spontaneous surges in viral repli- cation, while the incidence of the delta virus cute liver failure (ALF) is a complex infection seems to be decreasing rapidly. multisystemic illness that evolves after a Vaccination should reduce the incidence of Acatastrophic insult to the liver manifesting hepatitis A and B, while antiviral drugs should in the development of a coagulopathy and ameliorate replication of hepatitis B.
    [Show full text]
  • Campylobacteriosis
    Zoonotic Disease Prevention Series for Retailers Campylobacteriosis www.pijac.org Disease Vectors Campylobacteriosis is a bacterial disease typically causing gastroenteritis in humans. Several species of Campylobacter may cause ill- ness in livestock (calves, sheep, pigs) and companion animals (dogs, cats, ferrets, parrots). Among pets, dogs are more likely to be infected than cats; symptoms present primarily in animals less than 6 months old. Most cases of human campylobacteriosis result from exposure to contaminated food (particularly poultry), raw milk or water, but the bacteria may be transmitted via the feces of companion animals, typically puppies or kittens recently introduced to a household. The principal infectious agent in human cases, C. jejuni, is common in commercially raised chickens and turkeys that seldom show signs of illness. Dogs and cats may be infected through undercooked meat in their diets or through exposure to feces in crowded conditions. Campylobacter prevalence is higher in shelters than in household pets. Campylobacter infection should be considered in recently acquired puppies with diarrhea. Symptoms , Diagnosis and Treatment Symptoms of Campylobacter infection in humans typically oc- Antibiotic resistance has been documented among cur 2-5 days after exposure and include diarrhea (sometimes various Campylobacter species and subspecies. There- bloody), cramping, abdominal pain, fever, nausea and vomit- fore treatment should be under the direction of a ing. In the vast majority of cases, the illness resolves itself veterinarian. Typically, antibiotic therapy is reserved without treatment, generally within a week, and antibiotics are for young animals or pets with severe symptoms, but seldom recommended. Symptoms may be treated by in- treatment of symptomatic pets may be appropriate in creased fluid and electrolyte intake to counter the effects of households to reduce the risk of human infection.
    [Show full text]
  • Hepatitis A, B, and C: Learn the Differences
    Hepatitis A, B, and C: Learn the Differences Hepatitis A Hepatitis B Hepatitis C caused by the hepatitis A virus (HAV) caused by the hepatitis B virus (HBV) caused by the hepatitis C virus (HCV) HAV is found in the feces (poop) of people with hepa- HBV is found in blood and certain body fluids. The virus is spread HCV is found in blood and certain body fluids. The titis A and is usually spread by close personal contact when blood or body fluid from an infected person enters the body virus is spread when blood or body fluid from an HCV- (including sex or living in the same household). It of a person who is not immune. HBV is spread through having infected person enters another person’s body. HCV can also be spread by eating food or drinking water unprotected sex with an infected person, sharing needles or is spread through sharing needles or “works” when contaminated with HAV. “works” when shooting drugs, exposure to needlesticks or sharps shooting drugs, through exposure to needlesticks on the job, or from an infected mother to her baby during birth. or sharps on the job, or sometimes from an infected How is it spread? Exposure to infected blood in ANY situation can be a risk for mother to her baby during birth. It is possible to trans- transmission. mit HCV during sex, but it is not common. • People who wish to be protected from HAV infection • All infants, children, and teens ages 0 through 18 years There is no vaccine to prevent HCV.
    [Show full text]
  • Eosinophilic Gastroenteritis Complicating Perforation in a Hepatitis C Patient Treated with Direct-Acting Antivirals
    Case Study Clinical Case Reports International Published: 18 Feb, 2020 Eosinophilic Gastroenteritis Complicating Perforation in a Hepatitis C Patient Treated with Direct-Acting Antivirals Ming X Huang1, Chun N Li1, Ruo M Ke1, Zuo Q Zhang2, Zhe Zhu3 and Xiao M Peng1,4* 1Department of Infectious Diseases, Sun Yat-Sen University, China 2Department of Radiology, Sun Yat-Sen University, China 3Department of Medicine, University of California, USA 4Central Laboratory, Sun Yat-Sen University, China Abstract The Direct-Acting Antiviral (DAA) therapy of Hepatitis C Virus (HCV) infection has demonstrated excellent efficacy and safety profile. Based on large cohort studies, Serious Adverse Events (SAEs) are rare [1,2]. Here, we reported the first case of a patient with alcoholic liver cirrhosis super infected by HCV presenting with a SAE of Eosinophilic Gastro Enteritis (EGE) complicating acute perforation during daclatasvir plus sofosbuvir therapy. Abbreviations CT: Computed Tomography; DAA: Direct-Acting Antiviral; EGE: Eosinophilic Gastro Enteritis; HCV: Hepatitis C Virus; SAE: Serious Adverse Event Case Presentation A 58-year-old Chinese man with history of alcoholic liver cirrhosis (Child-Pugh A) more than 10 years had been diagnosed with HCV infection (serum HCV RNA 6.85 logIU/mL, genotype 6a) and was treated with daclatasvir plus sofosbuvir. (Velpanat composed of velpatasvir 100 mg plus sofosbuvir 400 mg) The patient’s virological response was achieved at week 7, but his peripheral eosinophils rose from normal baseline to 2.79 × 109/L (Figure 1). Since the patient was asymptomatic, OPEN ACCESS the dual therapy was continued. On September 24, 2017 (about at week 8), the man was hospitalized *Correspondence: due to sudden severe right upper abdominal pain, abdominal distention and a fever of 38.9°C.
    [Show full text]