SALMONELLOSIS (Salmonella food poisoning, enteric paratyphosis) A common bacterial cause of food-poisoning worldwide. Over 1800 food-poisoning serotypes.

SALMONELLOSIS (Salmonella food poisoning, enteric paratyphosis) A common bacterial cause of food-poisoning worldwide. Over 1800 food-poisoning serotypes of salmonella (bacterium) exist.

RABIES (Hydrophobia, Lyssa) AGENT: - Rhabdovirus which causes an acute almost invariably fatal disease. RESERVOIR AND INCIDENCE Worldwide distribution (

YERSINIA PESTIS (Plague, Pest, black death, pestilential fever) During the course of the disease, 25,000,000 people perished, a fourth of the population of the world. AGENT: a gram negative coccobacillus

LEPTOSPIROSIS [Weil's disease, Hemorrhagic jaundice (Leptospira icterohaemorrhagiae), canicola fever (L. canicola), dairy worker fever (L. hardjo)] AGENT : Spirochete, Leptospira. Pathogenic leptospires belong to the species Leptospira interrogans, which is subdivided into more than 200 serovars. The main natural reservoirs for human infection vary with serovar: L. canicola in dogs, L. hardjo in cattle, L. pomona in swine, and L. icterohaemorrhagiae in rats. RESERVOIR AND INCIDENCE Rats, mice, field moles, guinea pigs, gerbils, squirrels, rabbits, hamsters, reptiles, nonhuman primates, livestock, and dogs. In one study, 40 % of stray dogs were seropositive. TRANSMISSION: Handling affected animals, contaminating hands, or abrasions with urine, or aerosol

LYME DISEASE (Lyme arthritis, Bannworth's syndrome, tick-borne meningopolyneuritis, erythema chronicum migrans [ECM], Steere's disease) AGENT: spirochete, Borrelia burgdorferi RESERVOIR AND INCIDENCE First implicated in 1982 as agent in a 1975 epidemic of juvenile inflammatory arthropathy in Old Lyme Connecticut. Cases have been reported from 46 states and the annual number of Lyme disease cases has increased 18 fold from 497 to 8803. TRANSMISSION: Transmitted mostly by Ixodes dammini and other ixodid ticks (three host tick with a two to three year life cycle). Ixodes dammini has a broad range of hosts; adults prefer white tailed deer but will also parasitize dogs, horses, and humans. Larvae feed primarily on rodents, especially mice. Nymphs feed on all hosts and appears to be primarily responsible for transmission of the disease to people. Birds are an important reservoir and means of dispersal. Dogs appear to be at greater risk than humans.

BORRELIOSIS (Relapsing fever, tick-borne relapsing fever, spirochetal fever, vagabond fever, famine fever) A widely distributed bacterial infection spread from wild rodents by ticks or lice, with high fatality Tick-borne relapsing fever occurs in Africa, the Americas, Asia and possibly parts of Europe. The causative agents are Borrelia recurrentis and several other borrelia strains (bacterium). TRANSMISSION: Epidemic louse-borne infection is not considered zoonotic. Endemic tick-borne relapsing fever is transmitted from the natural wild rodent reservoir by tick bites to humans and dogs. Transovarial transmission in ticks occurs. Blood-borne person-to-person and intrauterine transmission have been reported.

CAMPYLOBACTERIOSIS (Vibriosis, vibrionic abortion) AGENT:
Campylobacter (Vibrio) fetus ss. jejuni, a gram negative, microaerophilic, curved, motile rod that is worldwide in distribution. RESERVOIR AND Campylobacter species can be found in pet and laboratory animal species. Transmission to humans is by the fecal-oral route and can produce an acute gastrointestinal illness. Symptoms include diarrhea, abdominal pain, fever, nausea, and vomiting.

MELIOIDOSIS (Pseudoglanders, Whitmore's disease) AGENT: Pseudomonas pseudomallei (Malleomyces pseudomallei, Actinobacillus pseudomallei ) --MOTILE, Gram negative rod RESERVOIR AND INCIDENCE Normal inhabitant of surface soil and water in Southeast Asia, and tropical areas. Recent studies have shown that the water of tanks in which exotic aquarium fishes were imported was contaminated. Occurs in wild rodents, goats, pigs, sheep. Also identified in Chimps, orangutans, and macaques. . TRANSMISSION: by inhalation from moist soil-water reservoir, by contact with contaminated soil or water thru overt or inapparent skin wounds, or by ingestion of contaminated feeds. Can be venereal in man.

TULAREMIA (Francis' disease, deer-fly fever, rabbit fever, O'Hara disease) AGENT - Francisella tularensis, a small pleomorphic, gram-negative, nonmotile rod or coccobacillus that can survive several weeks in the external environment. RESERVOIR AND INCIDENCE Common often fatal septicemic disease of rabbits, squirrels, muskrats, deer, bull snakes, sheep, wild rodents, cats and dogs. Major reservoirs are RABBITS, TICKS, MUSKRATS. Has been reported in NHP's at an urban zoo. Natural infection in laboratory animals and zoonotic transmission from them has NOT been reported. TRANSMISSION: handling tissue of infected animals (direct contact with UNBROKEN skin is sufficient). Reported human infections due to a cat bite and scratch and a NHP bite also reported. transmitted by biting insects inhalation, ingestion

RAT BITE FEVER (Streptobacillary fever, Haverhill fever, epidemic arthritic erythema, sodoku) AGENT: Gram negative, pleomorphic bacillus. Two different agents can cause disease: 1. Streptobacillus moniliformis (Haverhill Fever) *Named after a 1926 outbreak in Haverhill, Mass. attributed to contaminated milk. 2. Spirillum minus (Sodoku) RESERVOIR AND INCIDENCE Present in the oral and respiratory passages of a large number of asymptomatic rodents, including Rats and Mice. Incidence of disease appears to be low. Historically, wild rat bites and subsequent illness (usually small children) relate to poor sanitation and overcrowding. TRANSMISSION: Man infected by bite of infected rodent or via contaminated milk or food

PASTEURELLOSIS (Shipping or transport fever, hemorrhagic septicemia) AGENT: Pasteurella multocida, small, nonmotile, polymorphic, gram-positive bacilli RESERVOIR AND INCIDENCE inhabits the oral cavity and upper respiratory tract of many animals (Rabbits, rodents, dogs, cats, mice, birds, swine). Dogs and cats are frequently healthy carriers. TRANSMISSION: All animals and birds may be colonized by pasteurellas, and human infection occurs by wound infection from bites or scratches. Animal- to-animal transmission may occur by ingestion and inhalation case report of meningitis in a woman who kissed her dog (cultured positive for organism) and also had dental caries which was considered to be the route of infection

ROCKY MOUNTAIN SPOTTED FEVER
(American Tick Typhus, Tick-borne Typhus Fever) AGENT: Rickettsia rickettsii. RESERVOIR AND INCIDENCE Dogs, wild rodents and rabbits. TRANSMISSION: Ixodid ticks (especially Dermacentor) or their host species. Most rickettsias are obligate intracellular parasites of the gut cells of invertebrates and can only survive briefly outside living cells. Crushed ticks or mites and their feces may infect through broken skin. Transmission from tick bite occurs only after several hours of attachment.

RICKETTSIALPOX (Vesicular Rickettsiosis, Kew Gardens Spotted Fever) AGENT: R. akari RESERVOIR AND INCIDENCE House mouse is reservoir host; most commonly seen in rodent infested urban dwellings ie New York City and other Eastern U.S. cities. Rats and moles can also harbor the organism. Not identified as a natural disease in laboratory rodents. TRANSMISSION: Mite, Allodermanyssus sanguineus, transmits to mice or to man. Lab infections in humans via respiratory route have occurred but lab infections due to mite bite have not been reported

MURINE TYPHUS (Flea-borne Typhus Fever, Endemic Typhus Fever, Urban Typhus) AGENT: Rickettsia typhi RESERVOIR AND INCIDENCE natural pathogen of rats and mice. Other mammals including cats, and their ectoparasites have been found infected. Outbreaks continue to occur in U.S., especially Texas. Natural lab infections have not been reported but lab acquired infections in people handling experimentally infected mice have been documented. TRANSMISSION: transmitted by flea or lice (Xenopsylla cheopis, Nosopsyllus fasciatus) to rodents or man. Humans are infected by contamination of flea bites, broken skin or conjunctiva by flea feces. Domestic animals may transport the flea vector to humans. Inhalation of contaminated dust may be a route of infection.

Venezuelan Equine Encephalitis
Arthropod borne ARBOVIRUSES: GENERAL: In most man is an accidental host infected when arthropods feed on him. Therefore quarantine of wild caught animals and elimination of ectoparasites should prevent: Examples: TICK BORNE viruses: 1. Russian-Spring-Summer Encephalitis 2. Louping Ill MOSQUITO BORNE viruses, ie 1. DENGUE (Breakbone Fever, Dengue Hemorrhagic Fever) AGENT: Flavivirus, Flavidviridae RESERVOIR: nonhuman primates, occurs in Asia, Africa, Australia, the Caribbean including Puerto Rico, the Pacific Islands, S. Europe, S. America TRANSMISSION: mosquito vector (Aedes) DISEASE

HANTAVIRUS PULMONARY SYNDROME
Hantaviruses occur in rodent populations world-wide. Rats and mice have been implicated in outbreaks and infection of laboratory personnel has resulted from infected rats. The virus is shed in the respiratory secretions, saliva, urine, and feces of infected animals and is transmitted to humans On May 14, 1993, the New Mexico Department of Health was notified of 2 persons who had died within 5 days of each other. Their illnesses were characterized by abrupt onset of fever, myalgia, headache, and cough, followed by the rapid development of respiratory failure. Tests for Yersinia pestis and other bacterial and viral pathogens were negative. After additional persons who had recently died following a similar clinical course were reported by the Indian Health Service, the health services of Arizona, Colorado and Utah were contacted to seek other possible cases. Blood and tissue specimens were sent to the Centers for Disease Control and Prevention (CDC). The results were negative except for signals for the Puumala hantavirus.

The genus Hantavirus is a member of the family Bunyaviridae
The genus Hantavirus is a member of the family Bunyaviridae. Hantaviruses are further divided into genotypes. Representative viruses in each genotype are the Hantaan virus, the Seoul virus, the Puumala virus, and the Prospect Hill virus. Additional groups exist. Hantaan, Puumala, and Seoul viruses are known human pathogens; Prospect Hill has not been associated with disease. RESERVOIRS: Rodents are the primary reservoir hosts with each hantavirus appearing to have a preferential rodent host. The epidemiological characteristics of outbreaks of human disease and the severity for the infection are determined mainly by the rodent host. Available data strongly supports the deer mouse (Peromyscus maniculatus) as the primary reservoir of the newly recognized hantavirus Infected rodents shed large quantities of virus in saliva, urine, and feces for many weeks, but the duration and period of maximum infectivity are unknown.

Lymphocytic Choriomeningitis Virus
Arenaviridae Important zoonotic agent Wild mice principal reservoir host Laboratory mice & hamsters Horizontal transmission Urine, saliva and milk Vertical transmission

Acquired perinatally Persistent, asymptomatic, tolerant infection Lifelong viremia and shedding Disease 7-10 months old Emaciated Rough hair coat Hunched Death

Acquired after 1 week of life Viremia, without virus shedding Die acutely, or recover and eliminate virus Adult mice Subclinical

Human Clinical signs Fever, headache, myalgia, nausea, vomiting, sore throat, photophobia Differential diagnoses Influenza, mononucleosis, herpes encephalitis, tuberculous meningitis

Response to infection Depopulate for public health considerations Rederivation is not a viable option, due to in utero transmission

Sample Test Question Which of the following rodent viruses can infect and cause flu-like symptoms in people? (Circle all correct answers) Mouse hepatitis virus. Rat coronavirus. Lymphocytic choriomeningitis virus. Ectromelia. Enzootic diarrhea of infant mice.

Pneumonia Virus of Mice (PVM)
Paramyxoviridae Infects mice, rats and hamsters Natural infections are subclinical and short- lived Immuno-compromised mice Chronic pneumonia & eventual death

Rotaviruses Reoviridae Uncommon in colonies today
Associated with clinical disease Mouse Group-A rotavirus EDIM = epizootic diarrhea of infant mice Rat Group-B rotavirus IDIR = infectious diarrhea of infant rats

Rotaviruses Clinical signs Rat rotavirus may be zoonotic
Neonatal diarrhea Stunted growth, lethargy & distended abdomens Mortality low Adults – asymptomatic Rat rotavirus may be zoonotic

Pneumocystis carinii Protozoa vs. fungus
Ubiquitous, opportunistic microorganism Life cycle within the lung alveoli Latent infections in many species, including man Different organism in rats and mice, than in humans Normally nonpathogenic Airborne transmission

Pneumocystis carinii Clinical pneumonia is usually associated with pre- existing conditions Neoplasia, immunodeficiency, immature immune responses Treatment and Prophylaxis Trimethoprim-sulfa Albendazole Control Rederivation of infected colony

Pneumocystis carinii 10X 40X Organism clusters adhere to alveolar wall
Lungs: Enlarged and solid Firm and rubbery 10X 40X Organism clusters adhere to alveolar wall Capillary blockage Pulmonary insufficiency

Cryptosporidium muris
Protozoa, uncommon Epithelial brush border Mice - gastric colonization Rats - Intestinal colonization Zoonotic potential

Giardia muris Protozoa - Lumen of anterior small intestine
Infects young and adult mice and rats Low degree of pathogenicity, except in nudes Rough hair coat, lethargy, distended abdomen Diagnosis Pear-shaped trophozoites in SI Cysts in feces

Pinworms Common Can infect both mice and rats Usually asymptomatic
Heavy infections “associated with” Rectal prolapse, intussusception, enteritis, fecal impaction Can infect both mice and rats Syphacia obvelata – common mouse pinworm Syphacia muris – common rat pinworm Aspicularis tetraptera

Pinworms Syphacia spp. Direct life cycle – 11-15 days
Adults found in cecum and large intestine Eggs deposited on perianal region Infective 5-20 hours after release Diagnosis Cellophane tape test Banana shape Fecal exam is NOT reliable

Pinworms Aspicularis tetraptera Direct life cycle – 23-25 days
Adults found in large intestine, not cecum Eggs passed in feces Infective 5-8 days after excretion Diagnosis Fecal examination Football shape Cellophane tape test - NOT reliable

Pinworms Treatment = Anthelmintics Control Ivermectin Fenbendazole
Injection, “micro-dot,” misting, drinking water Sensitive mouse strains, eg. C57Bl/6 Fenbendazole Feed or drinking water Multiple treatments Control Rederivation, depopulation, isolation, strict sanitation

Tapeworms Hymenolepis nana = Dwarf tapeworm
Direct or indirect life cycle Clinical signs – heavy infection Retarded growth, weight loss, intestinal occlusion Small intestine Zoonotic potential

Tapeworms Hymenolepis diminuta Clinical signs Upper small intestine
Indirect life cycle Arthropod intermediate host Clinical signs Similar to H. nana Upper small intestine Zoonotic potential

Pediculosis = louse infestation
Polyplax serrata (mice) Polyplax spinulosa (rats) Sucking lice Direct contact transmission Adults - host anterior dorsum of host Eggs attach are base of hair Clinical signs Anemia, unthriftiness, debilitation Vector of disease transmission Examples: hemobartonella, tularemia, trypanosomes, rickettsia

Malocclusion Dental formula: I 1/1 C 0/0 P 0/0 M 3/3
Incisors grow continuously throughout life span

Mammary Tumors Common in aged mice and rats Can grow rapidly Rats Mice
Benign fibroadenoma Mice Malignant adenocarcinoma

Miscellaneous Alopecias
Bite wounds Male mice fight viciously Barbering Dominance behavior Shaved, nonerythematous appearance C57Bl/6 necrotizing dermatitis

Mycoplasmosis Mycoplasma pulmonis
Small, gram-negative, pleomorphic organism Lacks a cell wall Mice and rats are natural hosts Vertical and horizontal transmission Clinical signs Often subclinical Upper respiratory snuffling, chattering oculonasal discharge Sick rodent signs

Mycoplasmosis Pathology
Colonizes luminal surface of respiratory epithelium Purulent rhinitis, otitis media, tracheitis, bronchitis, bronchopneumonia Rat – marked hyperplasia of bronchus associated lymphoid tissue (BALT) Also other tissues, such as female genital tract Endometritis, pyometra, salpingitis, perioophoritis

Mycoplasmosis Control
Treatment with antibiotics (tetracycline) suppress overt disease, but is not curative Rederivation may not be successful due to in utero transmission Procure mycoplasma-free animals Rigid sanitation

Salmonellosis S. typhimurium, S. enteritidis Fecal-oral transmission
Clinical signs Sick rodent signs, diarrhea Pathology Splenomegaly Multifocal hepatic necrosis Control Prevent wild rodent contamination

Tyzzer’s Disease Clostridium piliforme (Bacillus piliformis)
Gram-negative, spore-former Hosts: mice, rats, other rodents, rabbits, horses, dogs Fecal-oral transmission Clinical signs Most often in weanlings Mice: diarrhea, body wasting sudden death Rats: abdominal distention diarrhea is uncommon Morbidity and mortality varies

AAALAC Association for Assessment and Accreditation of Laboratory Animal Care International
AALAS American Association for Laboratory Animal Science AC Animal Care, APHIS, USDA ACLAM American College of Laboratory Animal Medicine AGRICOLA National Agricultural Library’s Agricultural OnLine Access (USDA) APHIS Animal and Plant Health Inspection Service (USDA) ARENA Applied Research Ethics National Association ASLAP American Society of Laboratory Animal Practitioners AV Attending Veterinarian AVMA American Veterinary Medical Association AWA Animal Welfare Act AWIC Animal Welfare Information Center AWRs Animal Welfare Regulations (USDA)

LYMPHOCYTIC CHORIOMENINGITIS - LCM
AGENT: Arenavirus Of many latent viruses present in mice, only LCM naturally infects humans. LCM can easily be transmitted from animals to humans. Isolated by Armstrong and Lillie during investigation of a St. Louis Encephalitis outbreak in RESERVOIR AND INCIDENCE Worldwide in wild mice (M. musculus). This disease is principally confined to the eastern seaboard and northeastern states in the U.S. Wild mice infect the lab mouse. Mouse and hamster are the only species in which long term, asymptomatic infection is known to exist. *LCM virus is present in experimental mouse tumors which is a second source of infection for humans. This was first recognized in a transplantable leukemia of C58 mice. The disease can also be transmitted to laboratory animals via inoculation of infected tissue culture cells. The infection also occurs in guinea pigs, rabbits, rats, canines, swine, and primates. TRANSMISSION: Infection in mice is maintained by congenital infection followed by lifelong carriage and excretion of virus in saliva, urine, and feces. Human infections are probably from contaminated food and dust, the handling of dead mice, and mouse bites. Bloodsucking arthropod vectors such as ticks, lice, and mosquitos may transmit the disease. Person to person transmission does not occur.

BABESIOSIS (Piroplasmosis) AGENT: Babesiosis in humans is a rare intraerythrocytic infection caused by Babesia divergens and microti. RESERVOIR AND INCIDENCE Natural hosts for B. microti are various wild and domestic animals, particularly the white-footed mouse and white-tailed deer. With extensions of the deer's habitat, the range of human infection appears to be increasing. In the USA, the parasite has been found in coastal and island areas of the northeast and mid-Atlantic states as well as Wisconsin, Minnesota, and California. B. divergens occurs in Europe. TRANSMISSION: Humans are infected as a result of Ixodes tick bites, but transmission from blood transfusion has also been reported. Splenectomized, elderly, or immunosuppressed persons are the most likely to have severe manifestations.

AMERICAN TRYPANOSOMIASIS
(Chagas's Disease, Chagas-Mazza Disease, South American Trypanosomiasis) AGENT: Trypanosoma cruzi RESERVOIR AND INCIDENCE Dogs, cats, and guinea pigs are the main reservoirs for human infection. T. cruzi occurs only in the Americas; it is found from southern South America to northern Mexico, Texas, and the southwestern U.S. An estimated 12 million people are infected, mostly in rural areas, resulting in about 60,000 deaths yearly. TRANSMISSION: Humans are infected when the insect's feces become rubbed into the wound caused by the bite of an infected bloodsucking insect (triatomid) or when the conjunctiva, mucous membranes or abrasions become contaminated. After invading local reticuloendothelial cells, the trypanosome multiplies in the blood. Adaption of triatomid vector to the human domestic environment allows transfer of infection between animals, from animals to humans or from human to human. Transmission by blood transfusions from infected persons, congenital infection, breast milk and laboratory accidents are possible.

LEISHMANIASIS [Cutaneous leishmaniasis: Chiclero ulcer, espundia, pianbols, uta, and buba (in the Americas); oriental sore, Aleppo boil (in the Old World); Bagdad boil, Delhi boil, Bauru ulcer (in the Middle East). Visceral leishmaniasis: kala-azar] AGENT: The causative agents of cutaneous leishmaniasis are Leishmania mexicana and L. brasiliensis in the Americas, and L. tropica in the Old World; and of visceral leishmaniasis, L. donovani, L. infantum, and L. chagasi. RESERVOIRS AND INCIDENCE: The geographic distribution of the cutaneous disease is Texas, Mexico, Central and South America, India, Pakistan, the Middle East, southern Russia, the Mediterranean coast and Africa. The distribution of visceral leishmaniasis is poorly reported, but foci probably occur in the Mediterranean basin, the Middle East, India, China, Mexico, Central and South America, and Africa. Wild animals, dogs and humans serve as reservoirs. Domestic dogs may be an important reservoir for humans. Humans are the only known reservoir in India. TRANSMISSION: Sandfly vectors transmit cutaneous leishmaniasis. Person-to-person, congenital, and blood-borne transmission of visceral leishmaniasis are possible.

CAPILLARIASIS AGENT: The causative agents are Capillaria hepatica (hepatic form), C. philippinensis (intestinal form) and C. aerophila (respiratory form). RESERVOIR AND INCIDENCE C. hepatica and C. aerophila are very rare infections with isolated cases reported from North, Central and South America, Asia, and Europe. C. philippinensis is endemic in certain areas of the Philippines and cases have been reported from Thailand and Japan. Humans are the reservoir for C. philippinensis. With C. hepatica, rodents are the reservoirs. Cats and dogs are the reservoir for C. aerophila. Peromyscus maniculatus and Cletheronomys gapperi are the major hosts in North America. TRANSMISSION: Humans are infected by eating raw fish containing infective larvae. The worm parasite lives in the intestines of humans and autoinfection occurs. Human feces contain large numbers of ova which contaminate watercourses and infect freshwater fish. Humans may be infected by the ingestion of ova in the soil also.

TRICHINOSIS AGENT: Trichinella spiralis, an intestinal nematode. RESERVOIR AND INCIDENCE Swine, dogs, cats, rats and many wild animals. Worldwide. In the U.S., there has been a marked reduction in the prevalence of trichinosis both in humans and pigs; prevalence in commercial pork now ranges from nil to 0.7%. Fewer than 100 human cases are reported annually and usually have been as a result of eating homemade sausage and other meat products using pork, horse meat, or arctic mammals. TRANSMISSION: In the natural cycle, larvae develop into adult worms in the intestines when a carnivore ingests parasitized muscle. Pigs generally become infected by feeding on uncooked scraps or, less often, by eating infected rats. In humans, infection occurs by eating insufficiently cooked meat. In the epithelium of the small intestine, larvae develop into adults. Gravid female worms then produce larvae, which penetrate the lymphatics or venules and are disseminated via the bloodstream throughout the body. The larvae become encapsulated in skeletal muscle.

ANGIOSTRONGYLIASIS SYNONYMS: Angiostrongylosis, eosinophilic meningitis or meningoencephalitis (A. cantonensis), abdominal angiostrongylosis (A. costaricensis). ETIOLOGY: Two metastrongylids, Angiostrongylus (Morerastrongylus) costaricensis and A. cantonensis, are the etiologic agents. The first species is responsible for abdominal angiostrongyliasis, and the second one for eosinophilic meningitis or meningoencephalitis.The definitive hosts of both species are rodents; man is an accidental host. Both species require mollusks as intermediate hosts for the completion of their life cycle. The main definitive host of A. costaricensis is the cotton rat, Sigmondon hispidus, in which the adult nematode lodges in the mesenteric arteries and their branches on the intestinal wall. The first-stage larva emerges from eggs laid in the arteries, penetrates the intestinal wall, and is then carried with the fecal matter to the exterior. In order to continue their development, the first-stage larvae have to be ingested by a slug. Vaginulus ameghini, in which they change successively into second- and third-stage larvae. When the infective third-stage larva is ingested by a rodent, it seeks the ileocecal region, where it penetrates the intestinal wall and locates in the lymphatic vessels (both inside and outside the abdominal lymph nodes). In this location the larvae undergo two molts before migrating to their final habitat, the mesenteric arteries of the cecal region. Oviposition begins after about 18 days. and the first-stage larvae appear in the feces 24 days after infection (prepatent period). In man, an accidental host. the parasite can reach sexual maturity and produce eggs, but the eggs usually degenerate, causing a granulomatous tissue reaction.

The development cycle of A. cantonensis is similar to that of A
The development cycle of A. cantonensis is similar to that of A. costaricensis. The intermediate hosts are various species of land snails, slugs, and freshwater snails. The definitive hosts can become infected by ingesting infected snails, or plants and water contaminated by them with the third larvae. In addition, infection can occur as a result of consuming transfer hosts (paratenic hosts), such as crustaceans, fish, amphibians, and reptiles, which in turn have eaten infected mollusks (primary intermediate hosts). The definitive hosts of A. cantonensis are primarily various species of the genus Rattus. When they enter a rat's body, the third-stage larvae (which developed in a mollusk) penetrate the intestine and are carried by the circulatory system to the brain, where they undergo two more molts and become young adult parasites. From the cerebral parenchyma they migrate to the surface of the brain. They remain for a time in the subarachnoid space and later migrate to the pulmonary arteries, where they reach sexual maturity and begin oviposition. The eggs hatch in the pulmonary arterioles, releasing the first larva, which migrates up the trachea, is swallowed, and is eliminated with the feces. Mollusks are infected by ingesting fecal matter of infected rodents. In man, who is an accidental host, the larvae and young adults of A. cantonensis generally die in the brain, meninges, or medulla oblongata. The nematode can occasionally be found in the lungs.

GEOGRAPHIC DISTRIBUTION AND OCCURRENCE:
Abdominal angiostrongyliasis, caused by A. costaricensis, is a parasitosis described a few years ago in Costa Rica; it is one of the most recently recognized zoonoses. Human disease has also been confirmed in Honduras, El Salvador, and Brazil. Suspected clinical cases have occurred in Nicaragua and Venezuela. In Panama, the adult parasite was found in five species of rodents belonging to three different families. In the past few years, the parasite has been found in several specimens of Sigmodon hispidus in Texas, USA. Ozyomys caliginosus in Colombia; and slugs in Guayaquil, Ecuador. The parasitosis is probably much more widespread than is currently recognized. A. costaricensis has not been recorded outside the Americas. Human cases of parasitism by A. cantonensis have occurred in Thailand, Vietnam, Kampuchea, the Philippines, Indonesia, Taiwan, Japan, Australia, and several Pacific islands. The parasite is much more widely distributed, and its existence in rats has been confirmed in southern China, India, Malaysia, Sri Lanka, Madagascar, Mauritius, and Egypt. Until recently, the geographic distribution of A. cantonensis was thought to be limited to Asia, Australia, the Pacific islands, and Africa. However, in recent years its presence has been confirmed in Cuba, where infected rats (Rattus norvegicus) and mollusks have been found; likewise, five human cases of meningoencephalitis have been attributed to A. cantonensis in that country. It is believed that the parasite was introduced to the island some years ago by rats from a ship from Asia. In a study carried out on rat species (R. norvegicus, R. rattus, and R. exulans) on the Hawaiian and Society Islands, the parasite was found in more than 40% of the specimens captured. In Egypt, 32.7% of 55 specimens of R. norvegicus harbored the parasite. In the province of Havana, Cuba, 12 out of 30 captured R. norvegicus were infected. In view of the worldwide distribution of R. norvegicus and R. rattus, these rodents were examined for the parasite in Puerto Rico, London, and New Orleans, but the results were negative. Eosinophilic meningitis associated with infection by A. cantonensis has been recorded in several hundred patients in endemic areas.

HYMENOLEPIS NANA AGENT: Dwarf tapeworm, Hymenolepis nana - measures mm long. RESERVOIRS AND INCIDENCE: The animal reservoir is the house mouse, but humans can be both definitive and intermediate hosts. Worldwide occurrence in warm climates. TRANSMISSION: Gravid proglottids disintegrate and eggs pass in the feces and may be ingested by another human. Larvae then develop in the intestinal villi and pass to the lumen of the gut to become the adult forms. Dogs, cats and their fleas can be infected as well as grain beetles which can serve as intermediate hosts.

SPARGANOSIS SYNONYM: Larval diphyllobothriasis. ETIOLOGY: The second larval stage (plerocercoid or sparganum) of the pseudophyllidean cestode of the genus Spirometra (Diphyllobothrium, Lueheela). Several species of medical interest have been described: Spirometra mansoni, S. mansonoides, S. erinacei-europaei, S. theileri, and S. proliferum. These are the most commonly accepted species at the present time, but it should be noted that they are difficult to differentiate and that the taxonomy remains in doubt. The definitive hosts are mainly domestic and wild canids and felids. The development cycle requires two intermediate hosts. The first is a copepod (planktonic crustacean) of the genus Cyclops. which ingests coracidia (free, ciliated embryos) that develop from Spirometra eggs when they reach the water with the feces of dogs or cats (definitive hosts). In the tissues of the copepod, the coracidium turns into the first larva, or procercoid. When a second intermediate host ingests an infected copepod, the procercoid develops into a second larval form, the plerocercoid or sparganum. The plerocercoid larva can be harbored by many vertebrates, including amphibians, reptiles, birds, small mammals (rodents and insectivores), man, nonhuman primates, and swine. Fish do not become infected. Some researchers believe that the second intermediate host is usually an amphibian, but can vary according to region. Numerous species of vertebrates become infected with plerocercoids by feeding on amphibians, but they may also develop plerocercoids after ingesting water containing copepods infected by procercoids (first larva). Several animal species that are not definitive hosts function as paratenic or transport hosts, since the larvae they acquire by feeding on animals infected with plerocercoids encyst again after passing through the intestinal wall and migrating to other tissues. This transfer process is undoubtedly important in the life cycle; but the fact that many species of secondary hosts can be infected directly by ingestion of copepods containing procercoids is probably no less important. When the sparganum reaches the intestine of the definitive host, it attaches to the mucosa; in 10 to 30 days, it matures into an adult cestode, completing the cycle. The adult S. mansonoides reaches about 25 cm in length in the intestine of the definitive hosts (cat, dog). The sparganum found in the tissues of the secondary intermediate hosts and paratenic hosts, including man, varies from 4 to 10 cm in length.

SCHISTOSOMIASIS (Bilharzia, Bilharziasis) AGENT: Schistosomiasis infects more than 200 million persons worldwide. The causative agents are Schistosoma mansoni, haematobium, and japonicum. RESERVOIRS AND INCIDENCE: Humans are the reservoir for S. mansoni and haematobium. S. japonicum infects cattle, water buffalo, horses, dogs, cats, rodents and monkeys. Intermediate hosts are species of snails (Biomphalaria and Bulinus). S. mansoni occurs in Africa, South America and some Caribbean islands (including Puerto Rico); S. haematobium in Africa and the Middle East; and S. japonicum in China, Japan, the Philippines, and South East Asia. TRANSMISSION: Cercariae in contaminated water penetrate human skin, especially in irrigated fields or rivers. In the body the parasite migrates via the liver to the superior mesenteric vein where maturation takes place in about 6 weeks. Eggs are disseminated throughout the body via the blood, released into the intestinal lumen and excreted. In water miracidia develop and penetrate the snail, which in turn excretes cercariae into the water.

SALMONELLOSIS (Salmonella food poisoning, enteric paratyphosis) A common bacterial cause of food-poisoning worldwide. Over 1800 food-poisoning serotypes.

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Presentation on theme: "SALMONELLOSIS (Salmonella food poisoning, enteric paratyphosis) A common bacterial cause of food-poisoning worldwide. Over 1800 food-poisoning serotypes."— Presentation transcript:

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SALMONELLOSIS (Salmonella food poisoning, enteric paratyphosis) A common bacterial cause of food-poisoning worldwide. Over 1800 food-poisoning serotypes.

Similar presentations

Presentation on theme: "SALMONELLOSIS (Salmonella food poisoning, enteric paratyphosis) A common bacterial cause of food-poisoning worldwide. Over 1800 food-poisoning serotypes."— Presentation transcript:

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About project

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