Vibrio Cholerae, Plague, Rabies, Bartonella PDF

Vibrio cholerae,Plague,Rabies,Bartonella By Dr Ahmed Alyan Abdelaziz Mohammed lecturer of Tropical Medicine and Gastroenterology Faculty of Medicine South Valley University  MICROBIOLOGY AND EPIDEMIOLOGY Vibrio...

Vibrio cholerae,Plague,Rabies,Bartonella By Dr Ahmed Alyan Abdelaziz Mohammed lecturer of Tropical Medicine and Gastroenterology Faculty of Medicine South Valley University  MICROBIOLOGY AND EPIDEMIOLOGY Vibrio cholerae is a curved motile gram-negative bacillus. V. cholerae is a noninvasive intestinal pathogen. V. cholerae O1 and O139 serogroup organisms are the causes of epidemic cholera. Non-O1 and non-O139 V. cholerae can cause isolated cases of usually mild gastroenteritis. Cholera results from secretory diarrhea caused by the actions of cholera toxin (CT) on intestinal epithelial cells. CT is an adenosine diphosphate–ribosylating enzyme that leads to chloride, sodium, and water loss from intestinal epithelial cells. V. cholerae has an aquatic reservoir, particularly in brackish estuarine water. The fecal-oral transmission is associated with unsafe water and inadequate sanitation.  There are an estimated three to five million cholera cases, resulting in approximately 100,000 deaths each year. The current cholera global pandemic began in 1961 and represents the seventh in the histori-cal record. Cholera is now endemic in more than 50 countries. Cholera can lead to explosive epidemics and outbreaks. The current pandemic is caused by V. cholerae O1 El Tor organisms, with the largest burdens in South Asia, sub-Saharan Africa, and Haiti.  CLINICAL MANIFESTATIONS Acute severe watery diarrhea can result in death from dehydration within 6 to 12 hours of onset of clinical symptoms. Bowel movements during cholera can become progressively more watery, eventually resembling rice water with a fishy odor. Vomiting, ileus, and muscle cramps are common. The presence of fever should prompt consideration of additional diagnoses. Complications of cholera largely reflect those resulting from hypotension and hypoperfusion and may include acute renal tubular necrosis and stroke, usually in older individuals. Aspiration pneumonia from vomiting may also occur. Death from cholera almost always results from dehydration. DIAGNOSIS Cholera should be considered when an adult or child aged 5 years or older develops severe dehydration or dies of acute watery diarrhea in any area, or when an individual aged 2 years or older develops acute watery diarrhea in an area known to be endemic for cholera. Rapid antigen tests are available, including dipstick stool assays. Confirmatory microbiologic culturing permits definitive identification and assessment of antimicrobial resistance profiles.  MANAGEMENT The cornerstone of management is rapid assessment of the degree of dehydration, followed by prompt fluid restoration as well as vigorous monitoring and matching of ongoing fluid losses. Severe dehydration (>10% fluid loss), may require greater than 100 mL/kg of fluid replacement to restore euvolemia, ideally administered within the first 3 to 4 hours of clinical presentation. Moderate dehydration (5% to 10% fluid loss) may require 75 to 100 mL/kg of fluid resuscitation within the first 3 to 4 hours of clinical presentation. Individuals with no or mild dehydration may be treated with oral rehydration solution (ORS) alone or liquid ad libitum. Intravenous fluids are indicated for severe dehydration and in those unable to ingest adequateORS. Lactated Ringer’s solution supplemented with 5% dextrose (D5LR) (ideally supplemented with additional potassium) is an optimal choice for patients with cholera, although intravenous normal saline or normal saline supplemented with dextrose (and potassium)can also be used. Oral rehydration treatment should be encouraged among all individuals able to ingest,regardless of degree of dehydration, and regardless of potential ongoing administration of intravenous fluid.  ORS can be made in resource-limited settings by adding 12 tsp of table salt to 6 tsp of table sugar in 1 L of safe water, ideally supplemented with locally available potassium sources, such as coconut milk, bananas, or orange juice. Antibiotics play a secondary role in the treatment of individuals with cholera and usually involve administration of a macrolide or fluoroquinolone antibiotic. Tetracyclines can be used in non pregnant individuals older than 7 years in areas with confirmed susceptibility Antibiotics decrease the duration of diarrhea and may limit secondary transmission. PREVENTION Control primarily focuses on surveillance, case detection, fluid resuscitation and management, vaccination, and provision of safe water and adequate sanitation. Two oral killed cholera vaccines are currently commercially available and approved by theWorld Health Organization. Additional cholera vaccines are under development. Yersinia Species (Including Plague) DEFINITION Three human pathogens: Yersinia enterocolitica, Y. pseudotuberculosis, Y. pestis Zoonoses with multiple animal hosts, widespread in environment All have tropism for lymph nodes, but clinical illness and ecology differ EPIDEMIOLOGY Globally distributed but Y. pestis usually found within distinct ecologic foci. Y. enterocolitica, Y. pseudotuberculosis: fecal-oral transmission, enteric pathogens, more common in children, illness often self-limited. Y. pestis: vector borne, highly invasive, all ages, frequently fatal, potential bioterrorism agent.  MICROBIOLOGY Aerobic, gram-negative members of Enterobacteriaceae Growth at 37° C on MacConkey agar, sheep blood (Y. pestis, Y. pseudotuberculosis), Salmonella- Shigella media (Y. enterocolitica), and brain-heart infusion Automated identification systems may misidentify CLINICAL MANIFESTATIONS AND DIAGNOSIS Regional suppurative lymphadenitis, sepsis, or fulminant pneumonia with plague Bioterrorism mass exposure: fulminant pneumonia Enteritis and pseudoappendicitis with Y. enterocolitica, Y. pseudotuberculosis Reactive arthritis or erythema nodosum may follow diarrhea; HLA-B27 predisposes Culture of blood, stool, bubo, or sputum Acute and convalescent serology  THERAPY Immediate use of antimicrobial agents: lifesaving for plague or Yersinia bacteremia Plague: streptomycin, 1 g twice daily; gentamicin, 5 mg/kg once daily; or levofloxacin, 500 to 750 mg once daily, preferred. Y. enterocolitica, Y. pseudotuberculosis (aminoglycosides, tetracycline, fluoroquinolones) Antimicrobial agents generally unnecessary for enteritis or mesenteric lymphadenitis PREVENTION Safe handling and preparation of pork products Avoid unpasteurized milk and dairy products Reduce rodent harborage; control fleas on pets Avoid contact with rodents and sick animals Rabies (Rhabdoviruses) EPIDEMIOLOGY Rabies is one of the oldest human diseases, with the highest case fatality rate. Approximately 3.3 billion people live in regions where rabies is enzootic. An estimated 55,000 people die from rabies each year. Although all age groups are susceptible, rabies is most common in children younger than 15 years. Bites by rabid dogs cause 99% of human deaths globally. In the United States, bats account for most human rabies cases. Rabies virus transmission may also occur through tissue or organ transplantation. MICROBIOLOGY Rhabdoviruses are bullet-shaped, single-stranded RNA viruses of the order Mononegavirales,family Rhabdoviridae, and genus Lyssavirus. Rabies virus is the type species of the Lyssavirus genus.  DIAGNOSIS Development of an acute neurologic syndrome after the bite of a rabid animal is classically recognized in developing countries. Encephalitic rabies occurs in the majority of patients with fever, hydrophobia, aerophobia,agitation, autonomic overactivity with hypersalivation, coma, and paralysis. Paralytic rabies is characterized by ascending flaccid quadriparesis and coma. Antemortem diagnosis can be made by direct immunofluorescent staining of skin biopsy specimens, reverse-transcriptase polymerase chain reaction of saliva or skin biopsy, or detection of antirabies virus antibodies in serum or cerebrospinal fluid. THERAPY There is no proven antiviral therapy. Most patients with rabies virus infection die within a few days to 2 weeks after the onset of coma.  PREVENTION Annually, more than 10 million people receive rabies postexposure prophylaxis. After exposure to a rabid animal, prevention consists primarily of prompt wound cleansing. Postexposure prophylaxis consists of prompt administration of rabies immune globulin and rabies vaccine according to the Advisory Committee on Immunization Practices and World Health Organization guidelines. Bat rabies causes the majority of human cases in the United States, and postexposure pro- phylaxis depends on the type of exposure and availability of the animal for rabies diagnosis. Preexposure prophylaxis should be targeted to high-risk groups, including  Preexposure Vaccination Schedule 1. Vaccine: Human Diploid Cell Vaccine (HDCV) or Purified Chick Embryo Cell Vaccine (PCECV). 2. Doses: Three doses administered intramuscularly (deltoid muscle) on the following schedule: Day 0 (first dose),Day 7,Day 21 or 28. 3. Booster Doses: Booster doses are not routinely recommended for most individuals. Those with ongoing exposure risks should have periodic serologic testing (every 6 months to 2 years depending on risk level). A booster dose is given if rabies antibody titers fall below the acceptable threshold. Benefits of Rabies PrEP 1. Simplifies Postexposure Prophylaxis (PEP): If exposed, individuals who received PrEP require only two doses of rabies vaccine (on days 0 and 3) instead of the full four-dose series and do not require rabies immunoglobulin (RIG). 2. Provides Partial Immunity: Offers protection even if immediate access to PEP is delayed.  Indications for PEP PEP is recommended after: 1. Bites or scratches from animals suspected of having rabies (e.g., dogs, bats, raccoons, foxes). 2. Direct contact with saliva, neural tissue, or other potentially infectious materials from a rabid or untested animal. 3. Exposure to bats, especially if the contact was unnoticed or during sleep. Steps in Rabies PEP 1. Immediate Wound Care:Wash the wound thoroughly with soap and running water for at least 15 minutes. Apply an antiseptic such as iodine or alcohol to the wound. Avoid suturing the wound if possible, to allow better drainage. 2. Rabies Immunoglobulin (RIG):Administered only to individuals not previously vaccinated. Infiltrate as much RIG as possible directly into and around the wound. Any remaining RIG is given intramuscularly at a site distant from the vaccine injection site. Dosage: 20 IU/kg body weight for human RIG (HRIG) or 40 IU/kg for equine RIG (ERIG). 3. Rabies Vaccine :Administered to all exposed individuals, regardless of prior vaccination status, on specific schedules: Unvaccinated Individuals: Four doses (days 0, 3, 7, and 14). Immunocompromised individuals require a fifth dose on day 28. Previously Vaccinated Individuals: Two doses (days 0 and 3) without RIG. Vaccines: Human Diploid Cell Vaccine (HDCV) or Purified Chick Embryo Cell Vaccine (PCECV). Route: Intramuscular (deltoid muscle). 4. Additional Considerations :For high-risk exposures in rabies-endemic areas, PEP may be initiated even if the animal is unavailable for testing.If the animal is available and remains healthy after 10 days of observation (for domestic animals) or tests negative for rabies, PEP can be discontinued. Bartonella, Including Cat-Scratch Disease EPIDEMIOLOGY AND MICROBIOLOGY Fastidious, facultatively intracellular, pleomorphic gram-negative bacilli Transmission via feces of arthropod vectors or by direct inoculation into non intact skin Bartonella bacilliformis: endemic only in the Andes mountains; reservoir— humans, and possibly, an animal reservoir. Bartonella henselae: globally endemic; reservoir—cats; vector—cat flea; transmitted to humans usually via cat scratch. Bartonella quintana: sporadic outbreaks worldwide; associated with homelessness and other conditions of poor sanitation; reservoir—humans; vector—human body louse.  CLINICAL FEATURES Chronic bloodstream infections (for months) is a hallmark of Bartonella infections B. bacilliformis: biphasic illness; Oroya fever (acute phase) characterized by fever, hemolytic anemia, and high fatality rate when untreated; verruga peruana (late phase) characterized by crops of angioproliferative skin lesions with an evolution of stages B. henselae: cat-scratch disease (CSD): self-limited regional lymphadenopathy B. henselae: bacillary angiomatosis (BA): vascular proliferative disorder observed in patients with advanced human immunodeficiency virus (HIV) infection and other immunocompromising conditions; cutaneous BA, hepatic, and splenic bacillary peliosis (BP) B. henselae: blood culture negative endocarditis, usually in patients with preexisting valvular lesions B. henselae: cause of fever of unknown origin (FUO) in immunocompetent children, and in immunocompromised patients (HIV-infected and transplant recipients) B. quintana: trench fever: usually a self-limited febrile illness B. quintana: blood culture negative endocarditis; can occur in patients with normal heart valves B. quintana: bacillary angiomatosis (cutaneous, subcutaneous, osseous) B. quintana: cause of FUO in HIV-infected patients  DIAGNOSIS Difficult to culture Serology: mainstay for diagnosis, but cross-reactivity among Bartonella species common Histopathology: CSD—granulomatous inflammation; BA—vascular proliferation; Warthin- Starry or Steiner stain demonstrates Bartonella bacilli in tissue Polymerase chain reaction testing on tissue or blood.  THERAPY CSD: no treatment (self-limited); possibly azithromycin for severe CSD Endocarditis: doxycycline for 6 weeks and gentamicin for first 2 weeks; renal insufficiency common in Bartonella endocarditis, thus rifampin can be substituted for gentamicin in the setting of renal insufficiency. Bacteremia: doxycycline for 4 weeks and gentamicin for first 2 weeks BA/BP: doxycycline is first choice and erythromycin or azithromycin is second choice; in HIV-infected and transplant recipients, doxycycline is preferred due to tolerability issues and drug-drug interaction potential with erythromycin; duration of 3 months or longer for cutaneous disease and 6 months or longer for severe Bartonella infection (e.g., BP, central nervous system) Neuroretinitis: doxycycline and rifampin for 4 to 6 weeks PREVENTION Avoid arthropod vectors; eradicate body lice to reduce risk of B. quintana Avoid cat scratches, bites, licks, and cat fleas to reduce risk of B. henselae; control of cat flea infestation is important THANK YOU