Campylobacter and Helicobacter Presentation PDF

CAMPYLOBACTER and HELICOBACTER Dr. Nasr Jalboush  CAMPYLOBACTER Characteristic – S-shaped, spirally curved (one or more spirals), gram-negative, pleomorphic rods. – motile by a single polar flagellum at one or both ends, – microaerophilic (3%-5% CO ), aero...

CAMPYLOBACTER and HELICOBACTER Dr. Nasr Jalboush  CAMPYLOBACTER Characteristic – S-shaped, spirally curved (one or more spirals), gram-negative, pleomorphic rods. – motile by a single polar flagellum at one or both ends, – microaerophilic (3%-5% CO ), aerobic or anaerobic, and oxidase-positive. 2 – do not use carbohydrates. Eighteen species are recognized, but only two species, Campylobacter fetus (with two subspecies) and Campylobacter jejuni are pathogenic for animals. The generally nonpathogenic Campylobacter spp. are found on the mucous membrane of the genital and intestinal tracts.  CAMPYLOBACTER FETUS Strains of C. fetus comprise two subspecies, C. fetus subsp. fetus and C. fetus subsp. Venerealis Both subspecies possess a surface protein capsule. This high-molecular weight surface array protein is essential for virulence. It mediates resistance to serum killing and to phagocytosis by preventing the binding of serum C3b.  Subspecies venerealis Cause of bovine genital campylobacteriosis. In this disease, the organism can be found in the preputial cavity of the asymptomatic bull and the genital tract of the cow and heifer. The mode of infection is venereal; organisms are present in the semen of infected bulls The placenta and fetus may be invaded with occasional abortion at 5-8 months.  Subspecies venerealis If birth occurs, the newborn may only live for a few hours. In some individuals, the embryo may die and be resorbed. The infected placenta is usually hemorrhagic and edematous. The uterine infection causes a metritis that results in infertility, and the organism may be shed from the uterus for varying periods.  Subspecies fetus This organism occurs in the intestine o cattle and sheep and in the genital tract of infected sheep and cattle. The mode of infection is ingestion, directly or via fomites, but not venereally from the ram. After ingestion, there is hematogenous spread with infection of the uterine mucosa. it may cause abortion in cattle (sporadic) and in sheep (multiple).  Subspecies fetus The placenta and fetus may be infected, with abortions occurring late in pregnancy; fetuses may undergo autolysis, and there may be stillbirths. After expelling the fetus, ewes may develop metritis. The placenta may be hemorrhagic and edematous Necrotic foci in the fetal liver are characteristic.  Specimens Special methods are employed for the collection of cervical mucus and preputial secretions for culture. Fetal stomach contents, fetal tissues, and placenta may also be cultured. It is important that clinical materials be fresh. Campylobacter spp., do not survive outside the host for more than several hours unless protected from drying and sunshine. Filtration may be used to aid recovery; Campylobacter can pass through a 0.65-pm membrane filter.  Direct Examination Campylobacter fetus can be demonstrated (presumptively) in the fetal stomach contents by negative staining and by phase or dark-field microscopy. A fluorescent antibody reagent can be used to identify C. fetus in preputial washings, cervical mucus, and fetal stomach contents. A polymerase chain reaction (PCR) procedure has been used to detect subsp. venerealis in semen.  Laboratory Diagnosis Blood agar containing antibiotics to reduce growth of contaminants is satisfactory. For optimal recovery, plates are incubated at 37°C in an atmosphere of 10% CO2, 5% 02, and 85% N2. Fine pinpoint colonies are seen after 3-6 days of Incubation. Smears reveal small, gram-negative rods that assume various forms, short and long, both curved and S-shaped. Long, wavy filaments may be seen in some cultures.  Laboratory Diagnosis A fluorescent antibody procedure will identify C. fetus. Isolates of Campylobacter spp. have been identified based on 16S ribosomal RNA gene sequences. More recently, fluorescent amplified fragment length polymorphism (AFLP) fingerprinting, using the 16S rRNA sequences, has been found to be very specific in identifying various Campylobacter spp  Public Health Significance Campylobacter fetus subsp. fetus causes infrequent human infections, but not C. fetus subsp. venerealis. Among the infections seen are bacteremia, septic arthritis, endocarditis, septic abortions, peritonitis, salpingitis, meningitis, and thrombophlebitis. Patients with underlying disease, such as HIV infection, are particularly susceptible.  INFREQUENTLY PATHOGENIC SPECIES These include the following species with their sources (usually fecal); Campylobacter coli: Pigs and poultry; human infections. Campylobacter concisus: Human Infections. Campylobacter heIveticus Dogs and cats Campylobacter hyloileri: Pigs. Campylobacter jejuni subsp. doylei: human infections; has only been recovered from humans. Campylobacter Iari: Gulls and other avian species, dogs, and cats; human infections. Campylobacter upsaliensis: Dogs; human infections.  Campylobacter sputorum bivar bubulus: Cattle and sheep; human infections. Campylobacter sputorum bivar fecalis: Cattle and sheep: intestinal and genital tracts. Campylobacter sputorum bivar sputorum: Cattle and sheep: genital tract; human infections. The human infections referred to above are opportunistic. They include, but are not limited to, wound infections, diarrhea, proctitis, endocarditis, gastroenteritis, meningitis, sepsis. abscesses, and periodontal disease.  CAMPYLOBACTER JEJUNI Campylobacter jejuni occurs frequently as a commensal in the intestinal tract of many species of domestic and wild animals, including birds, poultry, dogs, and cats.  Pathogenesis and Pathogenicity Virulence factors associated with C. jejuni include adhesin, endotoxin, cytotoxin, and enterotoxin. Invasiveness has been associated with flagella and adhesin, which allow bacterial colonization. C. jejuni is capable of survival in the phagosomes. Enterotoxin activates adenylate cyclase, thus increasing intracellular levels of cyclic AMP. This results in large fluid loss into the lumen of the intestine, resulting in diarrhea.  Pathogenesis and Pathogenicity The production of cytotoxin results in local tissue destruction and abscess formation. Because many animals are carriers of C. jejuni, it Is often difficult to determine the significance of the organism in individuals with diarrhea. Observing large numbers of morphologically characteristic organisms in stained smears from rectal scrapings indicates pathogenic significance. Campylobacter jejuni causes infections characterized by diarrhea and enterocolitis in dogs, cats, sheep, goats, calves, laboratory animals, mink, ferrets, and other animals.  Pathogenesis and Pathogenicity Infections are more severe in younger animals. The organism also causes, infrequently, abortion in bitches, ewes, and cows and mastitis in cows. Campylobacter jejuni is the cause of avian infectious hepatitis of chickens and turkeys. It affects flocks with a low mortality, high morbidity, and chronic course with loss of condition; hemorrhagic and necrotic changes are seen in the liver.  CAMPYLOBACTER COLI Campylobacter coil occurs as a commensal in the intestinal tract of poultry and swine. It produces a heat-labile enterotoxin, it is rarely pathogenic. It is easily confused with C. jejuni. CAMPYLOBACTER UPSALIENSIS This species has been recovered from feces of both healthy and diarrheic dogs and cats and from feces of healthy children.  Laboratory Diagnosis incubation temperature is 42”C. Special measures such as filtration, the use of antibiotics in primary media, and below-surface sampling are used to reduce contaminants. Growth is slow, and colonies of the various species resemble (in size and morphology) those of C. fetus. They are slightly mucoid in appearance and are grey to pink or yellowish grey in color. In avian hepatitis, the characteristic morphology and motility of C. jejuni can be demonstrated in bile by phase microscopy. ‘this organism grows readily in a candle jar. Definitive identification of the various species Is based on growth characteristics, biochemical tests, and 16S rRNA gene sequences.  Species-specific deoxyribonucleic acid (DNA probes are being used in some diagnostic laboratories for the identification of Campylobacter recovered from feces. The fluorescent AFLP fingerprinting, using the 16S rRNA sequences, has been found to be very specific in identifying various Campylobacter spp. A commercial latex agglutination test is available for the identification of C. jejuni, C. coil, and other campylobacter spp. An ELISA is available for the serodiagnosis of C. jejuni infection.  Public Health Significance Campylobacter jejuni is the most frequent pathogen recovered from diarrheic stools associated with gastroenteritis in humans. The sources of the organism are many, including milk, poultry carcasses, feces of animal and human carriers, food and water contaminated by feces, and dog and cat feces with or without diarrhea. The course is usually 1-7 days with fever, abdominal pain, nausea, vomiting, and watery diarrhea with or without blood in the stool. Most infections are asymptomatic. Campylobacter coil, C. hyointestinalis, and C. upsaliensis cause infrequent foodborne diarrheic infections.  HELICOBACTER Organisms of the genus Helicobacter resemble campylobacter and were previously classified in the genus campylobacter. They are gram-negative, spiral and curved, motile (several sheathed flagella) and microaerophilic. At least 19 species of Helicobacter have been named, and all occur in the stomach or intestine of animals and humans worldwide.  HELICOBACTER Helicobacter spp. are carried in the stomach or intestine of many animals without causing apparent disease. They live beneath the mucous coating, where the PH may reach 7.4. It is estimated that the carrier rate of Helicobacter pylori for humans is 50%. It is thought that the inflammatory response, the accumulation of T cells, and the growth of Helicobacter lead to gastritis and sometimes gastric ulcers.  HELICOBACTER Transmission is considered to be mainly fecal/oral and oral/oral. They occur in the gastric mucus layer, and their capacity to break down urea with the production of ammonia and carbon dioxide with the consequent raising of the pH contributes to their survival.  Pathogenicity Helicobacter pylori is capable of causing chronic gastritis, and duodenitis and duodenal ulcer disease in humans. Gastric ulcer disease and gastric adenocarcinoma have been epidemiologically associated with this organism. This species has the potential to cause similar disease in cats.  Pathogenicity Other species implicated in gastric disease in humans are Helicobacter canis, Helicobacter felis, Helicobacter rappini, Helicobacter bills, and Helicobacter heilmannii (Helicobacter bizzozeronii). They can cause gastritis and more serious disease in dogs and cats. The following clinical signs have been attributed to Helicobacter infections in dogs and cats: – vomiting, regurgitation, abdominal pain, fever, diarrhea, anorexia, weight loss, and poor condition.  Laboratory Diagnosis Isolation and identification or demonstration of characteristic helical organisms, along with evidence of gastritis. Evidence of urease is supportive. Scrapings of the gastric mucosa are examined under phase microscopy for motile, helical-shaped organisms. These organisms can also be seen in smears and stained sections of gastric biopsies taken from areas of gastritis. Preparations may also be examined by electron microscopy.  Laboratory Diagnosis The isolation and identification of species of Helicobacter are complex and are not attempted in most veterinary diagnostic laboratories. They are microaerophilic, oxidase positive, do not use carbohydrates, and with the exception of H. canis, are catalase positive. Skirrow’s medium and chocolate agar with the addition of antibiotics are used for Isolation. Incubation for up to a week may be required for appreciable growth.