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Zoonotic Diseases

Please note: This is an informative page only. It is not meant to recommend treatment for either animal or human disease. If you have health concerns for your pet contact your Veterinarian. If you have health concerns for yourself contact your physician.

 

Afipia felis - See Cat Scratch Disease

 

 

ANTHRAX

(Malignant pustule, wool-sorters' disease, charbon, malignant edema, splenic fever) An acute bacterial infection of humans and animals which may be rapidly fatal. The disease occurs worldwide and is enzootic in certain African and Asian countries. It is an occupational hazard of persons such as wool-sorters, fellmongers, knackermen, farm workers and veterinarians in contact with infected animals or their products (e.g., blood, wool, hides and bones). The causative agent is Bacillus anthracis (bacterium).
RESERVOIR AND MODE OF TRANSMISSION:
All domestic, zoo and wild animals are potentially at risk of infection. Anthrax bacilli are released from infected carcasses and form resistant spores on exposure to air. These spores contaminate soil for many years. Humans are usually infected by inoculation from direct contact with infected animals, carcasses or animal products and contaminated soil. Inhalation or ingestion of spores may occur. Animals are infected from contaminated feed, forage, water or carcasses. Laboratory accidents have occurred.
INCUBATION PERIOD:
Humans. Cutaneous 3-10 days inhalation 1-5 days gastrointestinal 2-5 days. Animals. 1-5 days.
CLINICAL FEATURES:
Humans. Various forms include: 1. Cutaneous anthrax; localized ulceration and scab with fever and headache which may be followed within a few days by septicemia and meningitis. 2. Inhalation anthrax; fulminating pneumonia. 3. Intestinal anthrax; acute gastroenteritis with bloody diarrhoea. Animals. Peracute cases are found dead or moribund. Acute cases show fever, excitation followed by depression, incoordination, convulsion and death. Chronic cases show edema of throat, pharynx and brisket, especially in pigs.
PATHOLOGY:
Humans. Features include black scab (eschar) with edema, enlargement of regional lymph nodes and possibly septicemia; pneumonia and generalized hemorrhages. Animals. Carcasses should not be opened, hence necropsy is rarely carried out. Main features include failure of the blood to clot and hemorrhages throughout the body. The spleen is enlarged and softened. The subcutaneous swelling, mainly about the neck and throat of affected pigs and horses, contains gelatinous fluid. The blood contains very large numbers of B. anthracis.
DIAGNOSIS:
Humans. Identify B. anthracis in stained blood smears or by inoculation of laboratory animals. Culture swabs from wounds. Animals. As for humans. Specific antigen for anthrax may be found in animal products (e.g. hides) using a precipitin (Ascoli) test.
PROGNOSIS:
: Humans. Untreated cutaneous anthrax has a fatality rate of 5-20 Per cent and gastrointestinal anthrax of 25-75 per cent. Pulmonary anthrax is usually fatal. Animals. The condition is usually fatal in cattle unless treated early. Pigs and horses are more resistant.
PREVENTION:
Humans. Prohibit contact with infected animals and their products. Establish environmental and personal hygiene (e.g., ventilation and protective clothing) where a special risk exists. Treat wounds promptly and disinfect imports of hairs and wool. Vaccination may protect those occupationally exposed to risk. Apply strict laboratory safety measures. Isolate infected patients, with concurrent disinfection. Animals. Sterilize, or avoid using, meat and bone meal from high-risk countries for animal feed. Vaccinate livestock grazing in enzootic area. Dispose of infected carcasses safely and fence off areas contaminated by inadequately buried carcasses.
TREATMENT:
Humans. The mortality rate is high despite proper therapy, especially in pulmonary disease. Penicillin G, 2 million units IV every 4 hours, is the therapy of choice. tetracycline, 500 mg orally every 6 hours, may be used for mild, localized cutaneous infection. Animals. Penicillin injection of all animals showing fever after the first case is confirmed. This involves checking temperatures twice daily.
VACCINATION:
Humans. Offered to workers at risk. Animals. Non-encapsulated Stern strain vaccine can be used in all species of domestic animal. Annual vaccination of grazing animals using spore or alum precipitated antigen vaccine in areas of high risk is recommended.
LEGISLATION:
Humans. The disease is notifiable in most countries. It is a recognized occupational disease in some countries, including the UK. Animals. Notifiable in many countries with mandatory disposal of infected carcasses by burning or deep burial under lime. Opening of moving suspect carcasses is prohibited.

 

Bartonella - See Cat Scratch Disease

Bergeyella (Weeksella) zoohelcum

Species associated with infection - B. zoohelcum

Reported infections - wound infection, septicaemia, meningitis

Reported susceptibilities and treatments - cefotaxime, penicillins, ciprofloxacin, tetracycline

Notes - associated with cat and dog bites - previously classified as Weeksella zoohelcom

References - Reina, J., Borrell, N. (1992). Leg abscess caused by Weeksella zoohelcum following a dog bite. Clin. infect. Dis. 14, 1162-1163.

 

BLASTOMYCOSIS

SYNONYMS:
North American blastomycosis, Chicago disease, Gilchrist's disease.
ETIOLOGY:
Blastomyces dermatitidis, a dimorphic fungus existing in mycelial form in cultures and as a budding yeast in the tissues of infected mammals.
GEOGRAPHIC DISTRIBUTION:
The disease has been observed in the United States, eastern Canada, Zaire, Tanzania, South Africa, and Tunisia. Autochthonous cases may have occurred in some Latin American countries.
THE DISEASE IN MAN:
The incubation period is not well known; it possibly extends to several weeks or months. Blastomycosis is a chronic disease that principally affects the lungs. The respiratory symptomatology initially resembles influenzas purulent or bloody expectoration, weight loss, and cachexia, in addition to fever and cough, may develop later. If the infection remains localized, it can become asymptomatic. When it disseminates, it can cause subcutaneous abscesses as well as localized infections in several organs. Death frequently results in cases of untreated disseminated infection. The cutaneous form is commonly secondary to the pulmo-nary and is characterized by an irregular-shaped, scabby ulcer that has raised borders and contains minute abscesses. Lesions develop on exposed parts of the body.
THE DISEASE IN ANIMALS:
The highest incidence is observed in dogs around 2 years of age. The symptoms consist of weight loss, chronic cough, dyspnea, cutaneous abscesses, fever, anorexia, and sometimes blindness. The lesions localize in the lungs, lymph nodes, eyes, skin, and joints and bones. Of 47 clinical cases recently described, 72% occurred in large males. There were lesions of the respiratory tract in 85% of the cases.
SOURCE OF INFECTION AND MODE OF TRANSMISSION:
The reservoir is environmental, probably the soil, but the ecologic biotope has not been determined. Transmission to man and to animals is effected by aerosols; the fungal conidia are the infecting element. Persons at highest risk are those having the most contact with the soil. Dogs most frequently infected are sporting and hunting breeds.
ROLE OF ANIMALS IN THE EPIDEMIOLOGY OF THE DISEASE:
None. It is a disease common to man and animals. Cases of transmission from individual to individual (man or animal) are not known.
DIAGNOSIS:
Diagnosis is based on direct microscopic examination of sputum and material from lesions, on isolation of the agent in culture media, and on examination of histologic preparations. B. dermatitidis grows well in Sabouraud's culture medium or other adequate median it is most distinctive in its sprouting yeast form, and therefore the inoculated medium should be incubated at 37oC, since at ambient temperature the mycelial form of the fungus is obtained. B. dermatitidis in its yeast form (in tissues or cultures at 37oC) is characterized by a single bud attached to the parent cell by a wide base, from which it detaches when it has reached a size similar to the parent cell. In contrast, Paracoccidioides brasiliensis, the agent of paracoccidioidomycosis ("South American blastomycosis"), has multiple buds in the yeast phase. Serologic tests in use are complement fixation and gel immunodiffusion; the latter gives better results. It should be borne in mind that cross-reactions with Histoplasma and Coccidioides may occur. At present, the intradermal test is considered to have no diagnostic value.
TREATMENT:
Humans. Itraconazole, 100-200 mg/d orally, is now the therapy of choice for nonmeningeal disease, with a response rate of over 70%. Amphotericin B is given for treatment failures or cases with central nervous system involvement. Follow-up for relapse should be regularly made for several years so that therapy may be resumed or another drug instituted. Animals. Rare primary cutaneous disease may persist for months; these lesions should be removed surgically since blastomycosis responds poorly to therapy. Amphotericin B is considered the drug of choice, but treatment is of little avail once the disease is disseminated. The combination of amphotericin B and ketoconazole has been suggested to reduce the rate of relapse.
CONTROL:
As long as the ecologic biotope remains poorly defined, practical prevention methods cannot be established.

BRUCELLOSIS

(In humans: Mediterranean fever, undulant fever, Malta fever. In animals: contagious abortion, epizootic abortion, Bang's disease)
AGENT:
Brucella abortus: cattle, sheep Brucella canis: dogs Brucella melitensis: sheep, goats Brucella suis: swine
RESERVOIR AND INCIDENCE
Of the above species, Brucella canis is most likely zoonotic agent in the lab animal facility due to the extensive use of random source and lab bred dogs, in contrast to use of large domestic animals. Prevalence: 1 to 10% in dogs, throughout the U.S. B. canis is well adapted to dogs, and is not the subject of a large scale eradication program in the general dog population, as Brucella has been in other animals. Human brucellosis due to B. canis is uncommon but can be acquired from dogs; most cases resulted from contact with aborting bitches. In 1988, the CDC noted 96 cases of brucellosis reported in the U.S.: 22 from Texas and 20 from Calif.
TRANSMISSION:
Ingestion of unpasteurized milk Lab accidents Poorly defined transmission cycle in zoonotic diseases: contact with infected animals especially aborted fetuses, fluids or membranes, or urine. Possibly airborne.
DISEASE IN ANIMALS:
abortions are followed by immunity, though carrier state persists especially with secretions from the udder. infertility, testicular abnormalities, poor semen quality in dogs. inapparent infection may be common, as indicated by seropositivity.
DISEASE IN MAN:
Lymphadenopathy, splenomegaly, fever, headache, chills, orchitis, weakness, nausea, weight loss. The chronic form may assume an undulant nature, with periods of normal temperature between acute attacks; symptoms may persist for years, either continuously or intermittently. Antibiotics can effect a cure within one year in about 80% of cases. Case fatality if untreated is less than 2%.
DIAGNOSIS:
Rapid slide agglutination test is available. Blood culture and additional serologic tests used to confirm slide test results.
TREATMENT:
Single-drug regimens are not recommended because the relapse rate may be as high as 50%. Combination regimens of two or three drugs are more effective. Either (1) doxycycline plus rifampin or streptomycin (or both) (2) trimethoprim-sulfamethoxazole plus rifampin or streptomycin (or both) are effective in doses for 21 days. Longer courses of therapy may be required to cure relapses, osteomyelitis, or meningitis.
PREVENTION\CONTROL:
Quarantine and test Disposable gloves Chlorine, organic iodine, quaternary ammonium compounds are rapid bactericidal agents.

CAMPYLOBACTERIOSIS

(Vibriosis, vibrionic abortion)
AGENT:
Campylobacter (Vibrio) fetus ss. jejuni, a gram negative, microaerophilic, curved, motile rod that is worldwide in distribution.
RESERVOIR AND INCIDENCE
isolated from laboratory animals including dog, cat, hamsters, ferrets (>60 % in one study), nonhuman primates, rabbits, swine, sheep, cattle, and birds Although most cases of human campylobacteriosis are of unknown origin, infection after contact with sick animals has been well documented. *In most reports of pet to human transmission of C. jejuni, diarrheic puppies or kittens from pounds have been the source of infection. Pet birds, chickens, and kittens are implicated in other reports. A lab animal technician developed Campylobacter enteritis after feeding and cleaning up after a recently imported nonhuman primate. The organism was first isolated from nonhuman primates from Macaca fascicularis in 1979 and has since been reported in baboons, rhesus, patas, and marmosets. Can be shed for long periods of time in stool by asymptomatic carriers. Younger animals seem more likely to acquire the infection and hence may more commonly shed the organism.
TRANSMISSION:
Transmission is thought to occur by the fecal-oral route, through contamination of food or water, or by direct contact with infected fecal material. The organism has also been isolated from houseflies. At 40 C the organism is viable for three weeks in feces and milk, four weeks in water, and five weeks in urine. Campylobacter is shed in the feces for at least six weeks after infection. Infected children may transmit infection to puppies or kittens, which may then expose other children. Poultry and cattle are the main reservoirs for human infection, which is acquired by ingesting contaminated raw milk, undercooked chicken or other food contaminated in the kitchen.
DISEASE IN NONHUMAN PRIMATES:
Variable. the majority are asymptomatic carriers. Mild to severe enteritis may be seen accompanied by fever, vomiting, and mucus and blood in the feces. Bacteremia may occur complicated by meningitis or abortion. Most signs appear 1 to 7 days after exposure and affect primarily the jejunum, ileum, and colon.
DISEASE IN FERRETS:
Asymptomatic to proliferative colitis. Shed organisms for long period of time (> 16 weeks).
DISEASE IN OTHER ANIMALS:
Has also been shown to cause hepatitis in poultry, proliferative ileitis in hamsters, and abortion in ruminants. In all animals, it may be associated with diarrhea, especially when acting secondarily to virus infection.
DISEASE IN MAN:
Acute gastrointestinal illness, diarrhea with or without blood, abdominal pain, and fever. It may cause pseudoappendicitis and, rarely, septicemia and arthritis. Usually a brief, self-limiting disease. In humans the asymptomatic carrier state is rare. Reinfection is possible in both animals and man.
DIAGNOSIS:
1. Rapid diagnosis is done with dark field or phase contrast microscopy of fecal material. 2. This is confirmed by stool culture which requires a special selective growth media(CAMPY-BAP) and incubation at 43oC with 10% CO2, 5% O2 and 85% Nitrogen. 3. Warthin Starry stain and histo 4. Various techniques are being used to detect seroconversion to the antigens of Campylobacter.
TREATMENT:
Animals can be treated based on culture and sensitivity. Currently erythromycin is the drug of choice, but does not eliminate the carrier state. Tetracycline or ciprofloxacin are alternatives.
PREVENTION\CONTROL:
Vaccines provide partial protection of short duration and routine use is not recommended. Control is aimed at isolation of affected individuals and personal hygiene. An increased awareness of the potential of infection due to Campylobacter is of primary importance. Thoroughly cook all foodstuffs derived from animal sources, particularly poultry. Recognize, prevent, and control Campylobacter infections among domestic animals and pets. Wash hands after handling poultry and animal feces.

CAPNOCYTOPHAGA

AGENT:
Capnocytophaga canimorsus (formerly Dysgonic fermenter-2), a recently described aerobic, gram negative bacillus with unusual fermentation pattern.
RESERVOIR AND INCIDENCE
Found as part of oral flora of normal dogs and cats. C. canimorsus has been isolated from the mouths of 24% and 17% of normal dogs and cats respectively. Serious infections in man are most commonly reported in splenectomized or immunocompromised people, alcoholics, or persons who have chronic respiratory disease. More than 40 cases reported, many fatal, since first reported in 1976.
TRANSMISSION:
Contact, bite or scratch from dog or cat
DISEASE IN MAN:
can lead to cellulitis and overwhelming bacteremia, meningitis, endocarditis, septic arthritis, and DIC. The organism appears to have an affinity for the eye, causing angular blepharitis and severe keratitis. Accidental corneal inoculation occurred during a tooth extraction in a Poodle causing severe refractory keratitis in a veterinarian. The predisposition of the cornea to infection may be due to its avascularity and to the low concentrations of immunoglobulins and complement components in the tissue. Most serious disease and fatalities have occurred in splenectomized people. Case fatality rates of 4-27% have been reported.
DIAGNOSIS:
History, clinical signs, and culture. ORGANISM IS SLOW GROWING. May require 8 days of incubation. Micro exam of blood smear or buffy coat with gram stain to detect organisms.
PREVENTION/CONTROL:
Awareness, especially of high risk individuals Treatment of bite wounds, Penicillin G. (Treatment of high risk people even without sign of infection recommended.)

 

CAT SCRATCH DISEASE

(Cat Scratch Fever, Benign Lymphoreticulosis, Benign nonbacterial Lymphadenitis, Bacillary Angiomatosis, Bacillary Peliosis Hepatis)
AGENT:
Controversial, it is not currently possible to definitively name the causative agent responsible for CSD. Felt to be either Afipia felis, a gram-negative rod or Rochalimaea henselae and Rochalimaea quintana. Both are members of class Proteobacteria and both are intracellular parasitic bacteria.
RESERVOIR AND INCIDENCE
Associated with domestic cats throughout the USA, and worldwide. Over 6000 cases annually. Seen more often in men than in women . Have seen clusters of infection within families within a 2 to 3 week period, suggesting that shedding by cats may occur periodically. Other sources of infection have included scratches from other species including dogs, squirrels, and goats and from wounds induced by crab claws, barbed wire, and plant material.
TRANSMISSION:
90% of patients have been exposed to a cat. 75% of these have been bitten, scratched, or licked. Most affected individuals are <20 years of age. 75-80% of the cases of CSD are diagnosed between September and February with a peak incidence in December. 4 to 6% of the general population and 20% of veterinarians have positive skin test reactions to CSD antigen.
DISEASE IN ANIMALS:
Subclinical
DISEASE IN MAN:
Different distinct syndromes exist:

Typical CSD

A primary lesion, most common on neck or extremities, will develop in 50% of the cases and appear approximately 10 days after a bite or scratch. A pustule persists for 1-2 weeks. 10-14 days after the lesion appears, lymphadenopathy develops and usually regresses within 6 weeks. 30-50% of the enlarged nodes become suppurative. Of the approximately 65% who develop systemic illness, fever and malaise are the symptoms most often noted. The disease is usually benign and most patients recover spontaneously without sequelae within 2-4 months. Many unrecognized cases probably occur. Disease appears to confer lifelong immunity.

Atypical CSD

The atypical forms of CSD, which constitute 11% of all cases, are extremely varied. The most common, representing 6% of all cases, is Parinaud's oculoglandular syndrome (POGS), or granulomatous conjunctivitis with preauricular adenopathy. Other, atypical presentations include tonsillitis, encephalitis, cerebral arteritis, transverse myelitis, radiculitis, granulomatous hepatitis and/or splenitis, osteolysis, atypical pneumonia, hilar adenopathy, pleural effusion, erythema nodosum, erythema annulare, maculopapular rash, thrombocytopenic purpura, and breast tumor. Bacillary Angiomatosis Dermal BA presents in several ways. The commonest form is an enlarging red papule with some resemblance to a cranberry, often with a collarette of scale and sometimes with a suggestion of surrounding erythema. This type of lesion may be mistaken for pyogenic granuloma, unless fairly deep biopsy specimens are examined. These lesions begin as small papules and enlarge, occasionally becoming several centimeters in diameter and rarely ulcerating. They may be single or quite numerous. Another form of dermal BA is a deeper, subcutaneous nodule that appears flesh-colored and may be either fixed to subcutaneous tissues or freely mobile. Rarely BA may present as a dermal plaque. BA has been reported to occur in every organ system, including the brain, and is often difficult to differentiate from mycobacterial and fungal infections or malignancy without the use of biopsy. It is unclear if the personality changes, ranging from frank psychosis to depression, that have been described in association with BA represent CNS involvement or a neurotoxic product of this infection. Bacillary Peliosis Hepatis BPH, a vasoproliferative condition involving the liver of HIV-infected patients, is characterized by a proliferation of cystic blood-filled spaces surrounded by fibromyxoid stroma in which one can see bacteria similar to those seen in BA. Clinically these patients may or may not have visible bacillary angiomas. Their symptoms usually include fever, weight loss, and abdominal pain or fullness. Physical exam may reveal organomegaly. Laboratory studies usually demonstrate elevation of alkaline phosphatase and ç-glutamyltransferase levels out of proportion to those of aminotransferase and bilirubin.
DIAGNOSIS:
The sedimentation rate is elevated, the white blood cell count normal, and the pus from the nodes is sterile. ID skin testing with antigen prepared from the pus is positive. Excisional biopsy, usually performed to exclude lymphoma, confirms the diagnosis.
TREATMENT:
For CSD: Rifampin, ciprofloxacin, gentamycin, and trimethoprim-sulfa. Aspiration of suppurating nodes is recommended for relief of pain. Symptoms resolve without treatment in 2-4 months. BA and BPH respond to erythromycin, rifampin, or doxycycline. Therapy must be continue for 4-6 weeks to avoid relapse.
PREVENTION/CONTROL:
Education. Wash hands after handling cat. Wash cuts and scratches promptly and don't allow cat to lick open wound.

Cheyletiella

Cheyletiella spp mites
(Cheyletiellosis, Cheyletosis, "Walking Dandruff")

This article is taken from the Boxer Parade Magazine, Summer 1979 Vol 2 Issue 1

Although 5 different species of Cheyletiella have been differentiated on the basis of minute morphological detail, the species most often referred to as C. parasitivorax (the rabbit fur mite).  Cheyletiella spp have been reported from: rabbits, squirrels, birds, dogs, cats and man. Cheyletiella dermatitis is a mild, nonsuppurative mite-induced dermatitis produced by Cheyletiella spp. living on the surface of the skin. Significant Facts easily identified by 3 characteristics
 

  1. very heavy thick pedipalps, each armed with a heavy "claw". (gives the appearance of an extra pair of legs)
  2. comb-like appendage on the end of each foot (not claw)
  3. prominent peritremes (of respiratory function, look like "fish gills")

Cheyletiella rasguri is the common species affecting dogs, while Cheyletiella prasitovorax is the species found on rabbits. Both species of mites can interchangeably transfer to man, dogs, cats and rabbits. It is not yet clear how long the mites survive on another host.

Simple scurfy dandruff with pruritus in young puppies is highly suggestive of Cheyletiella dermatitis.

Life Cycle

EGG LARVA NYMPH I NYMPH II ADULT
white, attached by fine cocoon to base of hair
Hatches in 4 days		 (6 legs)
Whire, 7 1/2 days		 (8 legs)
White, 4 1/2 days		 (8 legs)
White to Yellow, 5 days
(8 legs)
Yellowish, moves rapidly
14 days
  • all stages occur on the host
  • adult female mite fastens eggs to hair (like louse nits)
  • egg hatches in about 4 days (six legged larva)
  • after moulting larva becomes eight-legged nymph
  • nymph moults again to adult form
  • complete cycle takes 3 to 4 weeks

Behaviour Of  The Mites

  • non burrowing obligatory mite
  • live in the keratin layer of the dermis
  • not associated with hair follicles
  • very active movement in dermal debris
  • when feeding, attaches firmly at 30" angle and engorges on a clear colourless fluid
  • thought at one time to feed on other mites leg. Demodex) and hence the name C. parasitivorax
  • repeated attempts to demonstrate this have failed and there is no indication that Demodex sp, or any other ectoparasite is attacked
  • off host survival is poor

The mite is highly contagious, especially between puppies, but man may be affected too. Adult dogs are usually lightly infected even when in direct contact with infected puppies and very few mites or eggs can be demonstrated in debris from their coats. In contrast to dogs, cats have milder skin reactions and do not have severe cattery infestations, but may be a source of human infections (Gething, 1973).

The mites do not burrow but live in the keratin layer of the epidermis and are not associated with hair follicles.  They move about rapidly in pseudotunnels in dermal debris, but periodically attach firmly to the epidermis, pierce the skin with their styletlike chelicerae and become engorged with a clear colourless fluid (Foxx and Ewing, 1969).

Clinical Signs

  • usually subclinical in rabbits and cats
  • extremely irritating to dogs and man
  • persistant pruritis with scurfiness
  • trauma of scratching may result in denuded lesions all over the body
  • one case reported excessive surfy dandruff but an otherwise normal appearing coat in a litter of five  Sealyham terriers

The course is chronic, affecting otherwise healthy individuals for many months. Infestation is most severe and generalized in two to eight week old puppies. Older individuals may be almost symptomless carriers.

On puppies it is usually found in the rump region. Infestation spreads over the back and head but eventually much of the body is affected. Cats tend to have milder, more diffuse lesions and are remarkably free of pruritus. The cat's daily licking and washing probably remove many mites. Affected animals have excessively scurfy, slightly oily coats. The white (or yellowish) mites and eggs together with the keratin scales produced by the epidermal reaction produce an appearance of severe "dandruff'. Except for the scaling there is remarkably little skin reaction per se.

Diagnosis

  • routine skin scraping
  • mites clear well and preserve in Berlese medium
  • sometimes find mites during routine microscopic examination of sodium nitrate fecal floatations, especially in cats where there may be many mites with no obvious clinical signs – closer skin examination in these cases may reveal many characteristic Cheyletiella sp mites.

Other mite infestations (Otodectes cynotis, Sarcoptes scabiei, Notoedres catti, Dermanyssus gallinae and Eutrombicula alfreddugesi) can be differentiated by microscopic inspection of the mites.

Treatment

Since all available references indicate success with a variety of insecticide treatments it appears as if the mite is highly susceptible to many chemicals. Removal of the mites has been reported with the topical use of Led-O-Sen, sulphur, benzyl benzoate·lindone solutions, and organo phosphate dips.

Thorough treatment of all animals on the premises is necessary.  Malathion, ronnel, lindane or carbaryl will be effective for dogs Pyrethrins, rotenone powder or limi-sulfur dips may be used safely on cats or rabbits. Treatment should be repeated three times at weekly intervals.

Although mites do not live very long off the host, a strong effort should be made to physically clean the premises, improve sanitation practices and spray the area thoroughly at least once with a good residual insecticide.

Promising results in control have been obtained by hanging appropriate numbers of dichlorvos fly strips in the general kennel area of pet shops with severe infestations.

All new animals should be carefully inspected and dusted or sprayed with an insecticide before being added to colony housed animal facilities.

Cheyletiella sp infection in man

  • mite commonly transmits from animal to man
  • human infestation may occur either by direct skin contact between man and animal or through clothing
  • most common site of infection is arms and torso
  • causes a very irritating itchy dermatitis
  • any insecticidal preparation for external parasites of man is likely effective in treatment leg. Lindane lotion- "Kwellada")

Human infestations vary in severity, but after direct contact with infested animals, grouped, erythematous macules form on the trunk and buttocks. These rapidly develop a central papule which becomes vesicular and then pustular, finally rupturing to produce a yellow crusted lesion which is frequently excoriated because of the intense pruritus. Although the lesions are severely inflamed, they are well demarcated from surrounding skin.  Older lesions have an area of central necrosis which is highly diagnostic.  Constant animal contact is usually needed to maintain human infections.  With no further infestation lesions subside in three weeks.

References

Carroll, H. F.: Cheyletiella dermatitis. In Kirk, R. W. (ed.): Current Veterinary Therapy V. W. B. SaundersCompany, Philadelphia, 1974. Soulsby, E. I. L.: Helminths, Arthropods and Protozoa of Domesticated Animals. The Williams 6. Wilkins Company, Baltimore, 1968. 

 

 

Chlamydia Psittici

(Ornithosis, Parrot Fever, Chlamydiosis, Psitticosis)
AGENT:
Obligate,intracellular organism with a unique development cycle and worldwide distribution Genus Chlamydia has only four species, many strains 1. Chlamydia trachomatis- humans, mice (Zoonotic potential not known) 2. Chlamydia psittaci- BIRDS, Mice, g. pig, rabbits, cats, frogs, ruminants 3. Chlamydia pneumoniae- humans 4. Chlamydia pecorum- ruminants
RESERVOIR AND INCIDENCE
The mammalian strains appear to be a zoonotic problem only rarely. 2 cases of human conjunctivitis reported from close association with cats with chlamydial pneumonitis and conjunctivitis. Birds are the main reservoir of human infection, however, 25% of human cases have no history of avian contact. Ovine strains may infect pregnant women.
TRANSMISSION:
Inhalation; dry feces produce highly infective aerosols Direct contact with feces or respiratory secretions May survive in dust for several months.
DISEASE IN ANIMALS:
There are many strains of C. psittaci which produce a diverse disease spectrum in animals, e.g., conjunctivitis, air sacculitis, pericarditis, hepatitis, meningoencephalitis, enteritis, urethritis, arthritis, and endometritis with abortion. G.I. infection results in enteric shedding of the organism. Latency - Well recognized feature of Chlamydia infection, i.e., the organism can cause inapparent infection or fulminant infection in the same host. In clinically healthy birds, stress can precipitate clinical signs and shedding of the organism.
DISEASE IN MAN:
Asymptomatic or clinical disease after 1-2 week incubation period. Fever, chills, myalgia, anorexia, headache, nonproductive cough. Pneumonitis or atypical pneumonia may be present. May see a toxic or septic form with hepatosplenomegaly, hepatitis, meningoencephalitis and cardiac involvement with endocarditis. Ovine chlamydial infection in pregnant women is life-threatening, causing late abortion and neonatal death and disseminated intravascular coagulation in the mother.
DIAGNOSIS:
fecal culture (rarely successful) serology (CF, IFA) [Note: African Grey Parrot, cockatiel, and budgie may remain serologically negative despite active infection.] ELISA-based tests for antigen in feces has proven reliable.
TREATMENT:
Tetracycline or Erythromycin.
PREVENTION/CONTROL:
Treatment with tetracycline Introduce birds into colony from psittacosis-free flocks or use chlortetracycline chemoprophylaxis. Protective clothing (masks, gowns, gloves). Wild caught birds should be placed on chlortetracycline during quarantine. In sheep, keep flocks closed or vaccinate annually. Isolate aborting ewes until discharges cease.

Cowpox

Description
The contagious virus responsible for Cowpox in cattle can also affect other species including humans, small wild mammals and cats. There is only one reported case of cowpox affecting a dog. Signs of the disease include skin lesions (nodules, scabs and ulcers), eye problems (conjunctivitis)  and respiratory signs (pneumonia). Cowpox in cats occurs mainly in Europe and Asia.

Cause
The cause of Cowpox is an orthopoxvirus. It is transmitted through a bite or skin wound and usually causes skin lesions, although respiratory and ocular signs may occur following viraemia. Cats are usually infected having caught infected rodents but direct transmission from cat  to cat, or human to human can occur. In cattle transmission is via milkers hands or teat clusters on automated milking machines.

The virus is resistant in the environment surviving many months under dry conditions.

Breed Occurrence
Dairy cattle are at greater risk than others.

In cats there is no breed predisposition to infection, but predators (eg cats)  that catch infected small wild animals (especially gerbils, ground squirrels, voles, wood mice) which act as a reservoir for the disease are at greater risk of contracting the disease.

Signs

 Typical signs of cowpox virus infection include :

  • Cattle
    • Incubation period about 3-6 days
    • Scabby pox lesions (1-2 cm) and ulcers on the teats and udder
    • Most cows in a herd will be infected
    • Secondary mastitis develops in some cases
    • Calves - get lesions in the mouth
    • Bulls - get lesions on the scrotum
  • Cats 
    • Many infected cats may not show any signs.
    • Widespread scabby skin lesions
    • Sometimes a single scabby  skin lesion
    • Conjunctivitis occurs in some cats
    • Mouth ulcers and vesicles occur in some cats
    • Usual site of the skin lesions initially  is the head, neck and foreleg, but generalised secondary nodules, ulcers and scabs form over a 4-5 day period and dry leaving bald patches which may or may not regrow hair.
    • If viraemia occurs the cat may develop:
      • Depression
      • High body temperature
      • Inappetance
      • Diarrhoea
      • Pneumonia if cat is immune-compromised - grave prognosis

Human Cowpox is rare (1-2 cases are reported per year in the UK). Cats are thought to be a main source of infection but direct contact with infected cattle is also a common source of infection.  Signs in humans are most likely to occur in people with poor immunity or pre-existing skin disease and they include :

  • Painful skin - with scabby lesions - usually on the hands or face
  • General malaise - if they are viraemic
  • Fever
  • Death - very rare

Complications
Secondary bacterial infections can occur, and viraemia causes generalised disease.

Diagnosis
Diagnosis can be made by :

  • Isolating Cowpox virus from scabs collected from skin lesions.
  • Measuring blood antibodies (fluorescent antibody test)

Treatment

Most cats and cattle recover without treatment.

  • There is no specific treatment for Cowpox virus, and no vaccine.
  • Antibiotics may help to control secondary bacterial infections. 
  • The environment should be disinfected with hypochlorite solution (bleach)

Prognosis
In cattle the prognosis is good because it produces a mild, localized infection in most individuals

Good in cats with skin lesions and no viraemia, but poor if severely affected and pneumonia develops

CRYPTOSPORIDIOSIS

AGENT:
Extracellular protozoal organisms - similar to coccidia. Genus: Cryptosporidium, it remains unsettled whether more than one species exists. Taxonomy of species somewhat controversial but considered to be infective across species lines.
RESERVOIR AND INCIDENCE
Rodents, birds (particularly turkeys and chickens), ruminants, fish, reptiles, cats, dogs, rabbits, NHP's. Children over 2 years of age, animal handlers, travelers, homosexual men, and close personal contacts of infected individuals (families, health care and day-care workers) may be particularly likely to be infected. More than a dozen outbreaks have been reported in day-care centers around the world. Two major waterborne outbreaks have been documented. Cryptosporidium antibodies were detected in the serum of 20 of 23 cats (87%) suggesting that the exposure rate may be high.
TRANSMISSION:
Fecal-oral transmission is from animals to humans or humans to humans; waterborne transmission is also important. Oocysts passed in stool are fully sporulated and infectious; infection occurs as a result of their ingestion. In humans and animals, the full life cycle occurs within a single host. The organisms attach to the microvillous borders of enterocytes of the small bowel and also are found free in mucosal crypts. The host cell membrane deteriorates, leaving the parasitic membrane in direct contact with epithelial cell cytoplasm. The organisms do not, however, invade the tissues.
DISEASE IN ANIMALS:
Severe watery diarrhea in neonatal calves and lambs. In turkeys and chickens, the parasites are reported to occur in the sinuses, trachea, bronchi, cloaca, and bursa of Fabricius. The respiratory disease causes coughing, gasping, and airsacculitis. In reptiles, cryptosporidiosis is frequently reported in association with postprandial regurgitation. The organism affects the GI mucosa, resulting in marked thickening of the rugae and loss of segmented motility.
DISEASE IN MAN:
In immunocompetent persons, infection varies from no symptoms to mild enteritis to marked watery diarrhea (up to 10 stools daily) without mucus or gross or microscopic blood. Low-grade fever, malaise, nausea, vomiting, abdominal cramps, anorexia and weight loss may occur. The infection is generally self-limited and lasts a few days to about 2 weeks. In immunologically deficient patients, the illness is characterized by profuse (up to 15L daily), cholera-like diarrhea and by fever, severe malabsorption, marked weight loss, and lymphadenopathy. In AIDS, infection may involve any part of the GI tract, and multisystemic involvement has been described, especially involving the respiratory tract.
DIAGNOSIS:
Diagnosis is by detection of oocysts in stool by a variety of flotation or concentration methods or by mucosal biopsy, followed by special staining methods that use modifications of an acid-fast stain (routine fecal staining methods do not detect the organisms). Three stools should be examined over 5 days. A fluorescein-labeled IgG monoclonal antibody test has recently become available to detect oocysts.
TREATMENT:
No successful treatment has been developed so far. Generally, no treatment other than supportive is needed in immunocompetent persons since it is self-limiting. In immunoincompetent persons, spiramycin, zidovudine (AZT), paromomycin, octreotide, and eflornithine have been reported of value.
PREVENTION/CONTROL:
Personal hygiene. Careful handwashing by those in contact with any animals with scours.

 

 

 

 

CUTANEOUS LARVAL MIGRANS

(Creeping Eruption)
AGENT:
Caused by the larvae of the dog and cat hookworms, Ancylostoma braziliense and Ancylostoma caninum. A number of other animal hookworms, gnathostomiasis, and strongyloidiasis are rarely also causative agents.
RESERVOIR AND INCIDENCE
Cutaneous Larval Migrans is prevalent throughout the tropic and subtropics. Human infection is common in SE U.S., particularly where people come in contact with moist sandy soil (e.g., beaches, children's sand piles) contaminated by dog or cat feces.
TRANSMISSION:
direct skin contact with larvae. soil to skin contact. contamination with animal feces.
DISEASE IN ANIMALS:
Same as Ancylostomiasis.
DISEASE IN MAN:
At the site of larval entry, particularly on the hands or feet, up to several hundred minute, intensely pruritic erythematous papules appear. Two to 3 days later, serpiginous eruptions appear as the larvae migrate at a rate of several millimeters a day; the parasite lies slightly ahead of the advancing border. The process continues for weeks or up to a year, and the lesions may remain severely pruritic, vesiculate, and become encrusted and secondarily infected. Without treatment, the larvae eventually die and are absorbed.
DIAGNOSIS:
Presumptive - Characteristic clinical manifestations. Etiologic - ID of agent by biopsy in skin section but this is usually very difficult to achieve. Most cases are really not confirmed. No valid serodiagnostic tests currently available.
TREATMENT:
Simple transient cases require no treatment. Albendazole or thiabendazole. Antihistamines and antibiotic ointments.
PREVENTION/CONTROL:
Minimize contact (e.g., wear shoes!). Decontaminate environment: 10 lbs/ 100 sq ft. sodium borate - gravel/clay dog run; 1% sodium hypochlorite solution - cement dog run. Prevent environmental contamination. Public health education.

DERMATOMYCOSES

(Ringworm, Dermatophytosis, Tinea, Trichophytosis, Microsporosis, Jock Itch, Athlete's Foot)
AGENT:
Organisms are subclassified into: 1. Geophilic - inhabit soil 2. Zoophilic - parasitic on animals 3. Anthropophilic - Primarily infects humans All can produce disease in humans. Grouped in three genera 1. Microsporum 2. Trichophyton 3. Epidermophyton
RESERVOIR AND INCIDENCE
Fungal spores remain viable for long periods on carrier animals and fomites. Exposure to reservoir hosts harboring different dermatophytes determines the type and incidence of infection in humans. Microsporum canis can be carried by up to 89% of nonsymptomatic cats. Up to 50% of people exposed to infected cats, both symptomatic and asymptomatic, have acquired infection. Pets may also acquire disease from humans. **T. mentagrophytes is most commonly transmitted to man from rodents, M. canis from dogs and cats, and T. verrucosum from cattle and horses.
TRANSMISSION:
Direct or indirect contact with asymptomatic animals or with skin lesions of infected animals Contaminated bedding Equipment Fungi in air, dust, or on surfaces of room (spores persist on contaminated surfaces)
DISEASE IN ANIMALS:
In rodents is often asymptomatic and not recognized until people are affected. In cats is often asymptomatic. Dogs often show classic skin lesions. Varying severity of dermatitis occurs with local loss of hair. Deeper invasion produces a mild inflammatory reaction which increases in severity with the development of hypersensitivity.
DISEASE IN MAN:
Often mild, self limiting; scaling, redness, and occasionally vesicles or fissures. Thickening & discoloring of nails. May show circular lesions which clear in the center forming a ring. Fungal infections in man are categorized as to the location on the body: 1. Tinea capitis - Scalp & hair 2. Tinea corporis - Body (extremities, arm and hand, are most often affected in infections acquired from lab animals.) 3. Tinea pedis - foot 4. Tinea unguium - Nails
DIAGNOSIS:
KOH mount of skin scrapings, Fungal culture
TREATMENT:
Macerated (moist softening and fissuring) stage- aluminum subacetate ("Domeboro") solution soaks with potassium permanganate for secondary infections. Athlete's feet may respond better to 30% aqueous aluminum chloride or the carbol-fuchsin paint than to antifungal agents. Broad spectrum antifungal creams and solutions containing imidazoles or ciclopirox) instead of tolnaftate and haloprogin help to combat diphtheroids and other gram-positive organisms present at this stage and alone may be adequate therapy. Dry and scaly stage- several topical creams, liquids, or lotions are recommended (miconazole, clotrimazole, ketoconazole, econazole, sulconazole, oxiconazole, ciclopirox or naftifine. Betamethasone dipropionate with clotrimazole is recommended for acutely inflamed tinea lesions. For severe cutaneous infections, griseofulvin or ketoconazole is recommended.
PREVENTION/CONTROL:
Screen newly received animals. Routine sanitization of contaminated environment, equipment, and caging. Gloves, protective clothing, wash hands after exposure.

DIPYLIDIASIS

AGENT:
Dipylidium caninum - common intestinal cestode of dogs. Gravid proglottids are "pumpkinseed" shaped.
RESERVOIRS AND INCIDENCE:
Dogs, cats, and their wild counterparts. Arthropods serve as intermediate hosts. These include the dog flea (Ctenocephalides canis), the cat flea (C. felis), and dog louse (Trichodectes canis). Cosmopolitan including the U.S.
TRANSMISSION:
Humans, dogs, and cats are infected by ingestion of arthropod intermediate hosts which harbor the cysticercoid larvae.
DISEASE IN ANIMALS:
Usually no severe pathology. Possibly mild digestive problems or perianal pruritus.
DISEASE IN MAN:
Slight symptoms, if any. Mild weight loss, perianal itching, diarrhea, vague abdominal pain.
DIAGNOSIS:
Recovery of gravid proglottids that are passed in the feces or that crawl out of the anus.
TREATMENT:
Niclosamide or praziquantel.
PREVENTION/CONTROL:
Screen animals. Treat infected animals. Eliminate ectoparasites. Teach proper handling of pets to children.

ECHINOCOCCOSIS

(Hydatidosis, Hydatid Disease)
AGENT:
Echinococcus granulosis - causes "cystic" disease. Echinococcus multilocularis - causes "alveolar" disease. E. vogeli - causes polycystic disease.
RESERVOIR AND INCIDENCE
The definitive host for E. granulosis is a carnivore (all of which, except for the lion, are Canidae) that harbors the adult tapeworm in the small intestine. Human infection with E. granulosus occurs principally where dogs are used to herd grazing animals, particularly sheep. The disease is common throughout southern S. America, the Mediterranean and Middle East, central Asia, and East Africa. Foci of endemicity are in eastern Europe, Russia, Australasia, India, and the UK. In North America, endemic foci have been reported from the western USA, the lower Mississippi Valley, Alaska, and northwestern Canada. The life cycle for E. multilocularis involves foxes as definitive host and microtine (e.g., voles and meadow mice) rodents as intermediate host. Domestic dogs and cats can also become infected with the adult tapeworm when they eat infected wild rodents. The disease in humans has been reported in parts of central Europe, much of Siberia, northwestern Canada, and western Alaska. One case has been reported in Minnesota. The principle definitive host for E. vogeli is the bush dog; the main intermediate hosts are the paca and spiny rat. Domestic hunting dogs are also definitive hosts, and serve as an important source of human infection. Cases have been reported in South America.
TRANSMISSION:
E. granulosis: Human infection occurs when eggs passed in dog feces are accidentally swallowed. E. multilocularis: Human infection is by accidental ingestion of tapeworm eggs passed in fox or dog feces.
DISEASE IN ANIMALS:
Usually no clinical signs except for enteritis in heavy infestations. In sheep, hydatid cysts cause considerable condemnation of meat and loss of production.
DISEASE IN MAN:
E. granulosis - Cystic hydatid disease A liver cyst may remain silent for 10-20 years or more until it becomes large enough to be palpable, to be visible as an abdominal swelling, to produce pressure effects, or to produce symptoms due to leakage or rupture. There may be right upper quadrant pain, nausea, and vomiting. The effects of pressure may result in biliary obstruction. If a cyst ruptures, anaphylaxis and death may result. If fluid and hydatid particles escape slowly, allergic manifestations may result. Rupture can occur into the pleural, pericardial, or peritoneal space or into the duodenum, colon, or renal pelvis. Dissemination of germinal elements may be followed by the development of multiple secondary cysts. Pulmonary cysts cause no symptoms until they leak; become large enough to obstruct a bronchus, or erode a bronchus and rupture. Brain cysts produce symptoms earlier and may cause seizures. Cysts in the bone marrow may present as pain or spontaneous fracture. The bones most often affected are the vertebrae and paraplegia may develop due to compression of the spinal cord. 20% of patients have multiple cysts. 15% of untreated patients eventually die. E. multilocularis - Alveolar disease The primary localization of alveolar cysts is in the liver, where they may extend locally or metastasize to other tissues. The larval mass has poorly defined borders and behaves like a neoplasm; it infiltrates and proliferates indefinitely by exogenous budding of the germinative membrane, producing an alveolus-like pattern of microvesicles. 90% of untreated cases die within 10 years. E. vogeli - Polycystic form of human hydatid disease. Symptoms are variable according to cyst size and location. The polycystic hydatid is unique in that the germinal membrane proliferates externally to form new cysts and internally to form septi that divide the cavity into numerous microcysts. Brood capsules containing many protoscolices develop in the microcysts.
DIAGNOSIS:
Immunoblot assay.
TREATMENT:
Currently the definitive treatment is surgical removal of cysts. Newly available chemotherapy (albendazole or mebendazole) may alter this position.
PREVENTION/CONTROL:
In endemic areas, prevention is by prophylactic treatment of pet dogs with praziquantel and prevention of feeding dogs offal.

 

Helicobacter

Spiral Bacteria in the Human Stomach: The Gastric Helicobacters

Andre Dubois, M.D., Ph.D.

Digestive Diseases Division, Department of Medicine,
Uniformed Services University of the Health Sciences Bethesda, Maryland, USA

 

During the past decade, Helicobacter pylori has become recognized as one of the most common human pathogens, colonizing the gastric mucosa of almost all persons exposed to poor hygienic conditions from childhood. It also is often found, albeit with a lower frequency, in groups of high socioeconomic status. H. pylori causes chronic active gastritis and is a major factor in the pathogenesis of duodenal ulcers and, to a lesser extent, gastric ulcers. In addition, the presence of this bacterium is now recognized as a risk factor for gastric adenocarcinoma and lymphoma. Nevertheless, most infections appear without clinical consequences. In this second decade of intensive research, it is important to understand why H. pylori is sometimes a dangerous pathogen, and to determine how it can be eradicated in those at highest risk for severe disease.

At the end of the 19th century, several types of spirochetes and spirilla were observed for the first time in the stomach of animals (1,2). Beginning at the turn of the 20th century, similar spiral bacteria were found in gastrectomy specimens from patients with gastric cancer and peptic ulcer disease (3,4). In addition, gastroenterologists and surgeons noted but could not explain the almost universal presence of antral gastritis in patients with duodenal ulcers and the frequent presence of atrophic gastritis in patients with gastric ulcer and cancer. Nevertheless, the possibility that peptic ulcer disease or gastric cancer might be caused by an infectious agent was generally discounted. The observation made in 1975 that gram-negative bacteria were present in 80% of patients with gastric ulcer (5) was largely ignored by the scientific community which, at the time, was busily developing potent antiulcer agents (6). Skepticism remained the overwhelming reaction to the 1983 reports describing the frequent association between antral gastritis and the presence of Campylobacter-like bacteria (7), as well as of their culture and isolation from patients with gastritis (8). A similar reaction followed the subsequent demonstration that these Campylobacter-like bacteria were present in almost all patients with gastric and duodenal ulcers, and were generally associated with antral gastritis (9). In the past decade, however, a number of studies have confirmed and extended these early observations. A consensus regarding the major role of this bacterium, now named Helicobacter pylori, in causing gastroduodenal ulceration was formally presented in 1994 (10). Furthermore, in June 1994, the International Agency for Research on Cancer Working Group stated , "H. pylori plays a causal role in the chain of events leading to cancer," referring to adenocarcinoma and lymphoma of the stomach as well as to the more benign mucosal-associated lymphoid tissues (MALT) (11-13).

An important consequence of the considerable interest generated by these clinical observations is that extensive bacteriologic and molecular studies have been performed on this bacterium and similar organisms. 16S rRNA gene sequence analysis has revealed important differences between H. pylori and the closely related Campylobacter, Flexispira, and Wolinella genuses. These differences have necessitated the creation of the genus Helicobacter, which, to date, includes eight gastric, three intestinal, and two hepatic species (14). Each of these Helicobacter species colonizes different, or a spectrum of, mammalian species.

This review summarizes our current knowledge of the two Helicobacter species that have been observed in the human stomach and reported on extensively in the literature: H. pylori, the type strain, and H. heilmannii, also known as Gastrospirillum hominis (15,16).

Characteristics of Gastric Helicobacters Observed in Humans

H. pylori, a gram-negative bacterium with a curved, spiral, or gull-wing shape, is 2.5 to 3.5 µm long and 0.5 to 1.0 µm in diameter and has a periodicity of 1 to 2µm. It has smooth surfaces, and one to six polar-sheathed flagellae emerge from one of its rounded ends. Since it is morphologically similar to C. jejuni, it was initially named "pyloric Campylobacter" and subsequently C. pyloridis and C. pylori before finally being named H. pylori. This organism colonizes only the non-acid-secreting mucosa of the stomach and is not found where parietal cells are numerous. Thus, it may be observed in the gastric antrum and the cardia, but also in the corpus, when atrophic gastritis is present, and attached to the gastric epithelial cells found in the duodenum, when gastric metaplasia is present.

G. hominis (H. heilmannii) is tightly spiraled, and is 3.5 to 7.5 µm in length and 0.9µm in diameter; it has a periodicity of 0.8 to 1 µm and up to 12 flagellae at each pole. 16S rRNA indicates that this organism belongs to the genus Helicobacter, and is more closely related to a Helicobacter sp. isolated from the stomach of cats (H. felis) than to H. pylori (17). The name H. heilmannii was proposed in honor of the late German pathologist Heilmann. However, the subsequent examination of the rRNA of different clinical isolates indicates that there is enough heterogeneity among isolates tentatively identified as H. heilmannii that it is premature to propose an official name (17) . This bacterium colonizes only the parietal cell area of the gastric mucosa and may be found within parietal cells (18,19).

Diagnosis

H. pylori infection may be diagnosed by harvesting gastric biopsy specimens during endoscopy, by culturing and isolating the bacterium under microaerobic conditions (90% N2, 5% O2, and 5% CO2), and by characterizing the enzymes (urease, catalase, and oxidase) it produces. Visualization of the bacterium by light microscopy on slides stained with hematoxylin and eosin, Gram, Giemsa, Genta, or Warthin-Starry stain is also of great benefit since it allows the concurrent diagnosis of the extent of the antral chronic-active gastritis that H. pylori causes. However, because H. pylori colonization is focal, negative biopsy results do not exclude the possibility of infection in areas not sampled. Infection also may be diagnosed by determining plasma and salivary immunoglobulin (Ig) G or IgA levels with enzyme-linked immunosorbent assays (20,21). This latter technique is noninvasive, specific, and sensitive and is believed to reflect the mucosal and systemic immunity induced by H. pylori infection.

Two other tests, which rely on the production of urease, also can be used to identify H. pylori. One is the CLO (for Campylobacter-like organisms) test, which is performed by placing a mucosal biopsy specimen in medium containing urea and a pH- sensitive dye that changes color in the presence of OH- ions. The second test is the noninvasive 14C or 13C breath test following the oral administration of 14C- or 13C-urea. Neither of these tests is specific for H. pylori since G. hominis, which generates urease, also gives a positive reaction. Until specific methods based on the polymerase chain reaction (PCR) amplification of 16S rRNA (17) become widely available, the diagnosis of G. hominis infection must rely on histologic morphologic characteristics; histologic identification must be confirmed by transmission electron microscopy since other spiral organisms, e.g., Flexispira rappini, also may be present in the stomach of humans (22).

Epidemiology

The seroepidemiology of H. pylori has been extensively studied in the United States and in other countries (23). The high frequency of seropositivity (up to 100% in some age groups in Albania) and acquisition of the infection during infancy are characteristic of disadvantaged socioeconomic groups living in crowded or poor hygienic conditions and appears to be independent of gender and ethnic origin. In adults of higher socioeconomic groups, the rate of seroconversion is estimated at 0.5% per year, although the frequency of seropositivity increases with age and may be as high as 40%. A longitudinal study has indicated that the high frequency of seropositivity in older adults might be due to a higher rate of H. pylori infection in Western countries in the years between the two world wars than during recent years (cohort effect) (24). Alternatively, the increase in frequency of infection in older adults might be due to years of low but cumulative risk for infection. Although the route of transmission for this infection is not known, the contamination of drinking water may play a role in certain developing countries (25). In the United States and in other regions, direct contact and/or consumption of food or water contaminated by saliva (26), gastric contents, or feces (27) may be major factors. The recent observation that H. pylori can be isolated from cats (28) suggests that transmission from pets to humans (or humans to pets) is also possible.

The epidemiology and route of transmission of G. hominis are largely unknown. The frequency of this infection appears to range from less than 1% of the population in industrialized countries (29) to 3% to 8% in developing countries (30). Although the detection of spirilla in the stomach of cats and dogs suggests possible transmission from pets, marked morphologic differences exist between these spirilla and the organism found in the stomach of humans.

Pathogenicity

H. pylori is considered a pathogen because its presence is always associated with chronic active gastritis, and eradication of the bacterium is always followed by resolution of gastritis. In addition, nearly all patients with duodenal ulcer disease have H. pylori gastritis, and ulcer relapse is exceptional after H. pylori eradication. Thus, the presence of H. pylori seems necessary for the production of duodenal ulcers, with the exception of ulcers attributed to the use of nonsteroidal antiinflammatory agents or to the Zollinger-Ellison syndrome (10). The association with gastric ulcers is not as strong, although H. pylori infection is present in 80% of patients with gastric ulcers who do not consume nonsteroidal anti-inflammatory agents (10). However, most H. pylori-infected persons do not report any clinical symptoms. This may be because these persons are colonized by less virulent strains or because other host or bacterial cofactors are required for overt disease.

In addition, three prospective cohort studies have demonstrated that H. pylori-infected persons have an increased risk of developing intestinal-type, but not undifferentiated, gastric adenocarcinoma (10). In fact, the association of H. pylori with either gastric ulcer or gastric cancer may be underestimated in these studies: the atrophic gastritis that follows long-term infection makes the gastric niche less hospitable for the bacterium, which may either eliminate H. pylori or make it difficult to detect. Nevertheless, atrophic gastritis per se is believed to be a precancerous lesion that leads to carcinogenesis without the presence of H. pylori.

The pathogenicity of G. hominis is unclear. The organism has been associated with upper gastrointestinal complaints, and its carriage is generally accompanied by gastritis, although the inflammation and gastric atrophy are less than noted with H. pylori (31,32). In addition, G. hominis was observed in gastric cancer patients (3) as well as in patients with only minimal gastritis (29). In this relatively small number of cases, the frequent concurrent infection with H. pylori makes interpreting the respective pathogenic role of either bacterium difficult. It is probable that G. hominis will turn out to be at least somewhat pathogenic, as it makes urease and products of urease action that have been implicated in inflammation.

Colonization and Virulence Factors

H. pylori multiplies with great efficiency in the hostile environment within the stomach but survives poorly in the gastric lumen; it is mainly found where the pH ranges between 4 and 7, i.e., under the mucous layer and in close proximity, or even attached, to gastric superficial epithelial cells. The virulence and the ecologic niche of G. hominis are unknown, although its presence within parietal cells of patients with gastrointestinal complaints (18,19) suggests that it is even more resistant to acid than H. pylori.

The production of urease was the first putative colonization or virulence factor studied. The production of this enzyme is shared by the two organisms, and it may explain their extraordinary ability to survive in an environment previously considered sterile because of the presence of proteolytic enzymes, as well as the low pH of gastric contents. Because the ecologic niches of these bacteria are rich in urea, urease generates OH- ions that neutralize gastric acid. Although the neutralization of gastric acid benefits the two bacteria, the production of hydroxide ions also is toxic to gastric epithelial cells in vivo, as indicated by in vitro experiments (33).

Two other important virulence factors shared by H. pylori and G. hominis are their spiral shape and the motility of their flagellae, which render them resistant to peristaltic flushing of the gastric contents and enable them to persist in the mucous layer. Because G. hominis appears to infect fewer persons than H. pylori, a more important role might be attributable to characteristics that are unique to H. pylori; these include the production of other enzymes (catalase, oxidase, protease, and phospholipase), as well as the synthesis of specific adhesin proteins that enable them to adhere to mucous and epithelial cells, both in vivo and in vitro (34-36).

The putative virulence factor of H. pylori that has commanded the most attention during the past few years has been its vacuolating cytotoxin (vacA gene product). Intragastric administration of the toxin to mice causes some (but not all) of the tissue damage seen in H. pylori-infected persons (37). In addition, cytotoxin production is highly correlated with the production of a high molecular weight (120 to 128 kilodaltons) major protein antigen that is called cytotoxin-associated protein (cagA) and is not the toxin itself (38).

Diversity of H. pylori

H. pylori isolates may differ with respect to each of the virulence factors described above; this diversity is likely to contribute to variation in colonization or disease. For example, urease-negative strains have been isolated, and the vacuolating cytoxin is produced by only a subset of H. pylori strains (vacA+ or tox+ strains)(39-41). This observation is probably clinically relevant because most or all strains from duodenal ulcer patients, and many strains from gastric cancer patients, produce cytotoxin, whereas only a fraction of strains from patients with gastritis alone produce the cytotoxin (42,43). This phenotypic diversity is mirrored in great diversity on the DNA level. Thus, only cytotoxin-producing strains contain the gene for this cytotoxin-associated protein (cagA)(38,42), although genetic tests have shown that cagA protein is not needed for toxin production (44). Strains that do not produce the 128-kDa cagA protein generally lack the entire cagA gene and additional neighboring genes. Although the function of the cagA region is unknown, its presence or absence is easily scored by hybridization or PCR and thus serves as an easy marker for probable cytotoxin production and possible virulence of H. pylori strains. Additional virulence factors are likely to be present. For example, another recently discovered region constitutes at least 21 kilobases of the H. pylori genome in hybridization experiments, and its presence is highly correlated with the presence of cagA: 39 of 40 strains lacking cagA also lacked this region, and 50 of 52 strains containing cagA contained this region. This newly discovered region is being called cagII, and the effort to sequence it is nearly complete (D. E. Berg, pers. comm.). Preliminary searches have identified several open reading frames with strong homologies to virulence functions from other microbes (45).

In addition to these extensively studied genes, genetic diversity of various H. pylori strains can be demonstrated by the use of two sensitive, efficient, and reliable PCR-based methods (46,47). This approach is particularly useful because it allows tracing of strains in epidemiologic studies.

Infection and Immune Response

One of the most puzzling aspects of gastric infection with H. pylori is its persistence despite intense local and systemic immune responses. These immune responses are extremely complex and vary among infected humans. The systemic response is characterized by a marked increase in plasma IgG, which remains present for months after the infection has been cured. The local response includes the production of IgA, which binds to the surface antigens of H. pylori in vitro and coats the bacterium in vivo. In addition, infection is consistently associated with an intense inflammatory response and the infiltration of cells into the gastric mucosa. Although polymorphonuclear cells are often present, most cells in such infiltrates are mononuclear cells. Both B and T cells are present, and recent studies have indicated that the natural killer activity of peripheral blood lymphocytes can be increased by H. pylori, possibly by its stimulating the production of interferon and other cytokines (48). Thus, the long-term carriage of the infection may be related to the ability of the bacterium to influence the T-cell response. Fragmentary evidence also suggests that this infection can be abortive and cure spontaneously without the use of antibiotics (A. Dubois and D. E. Berg, unpublished).

On the other hand, the mucosal response may promote colonization, as indicated by the observation that patients with acquired immunodeficiency syndrome (AIDS) tend to have a lower rate of infection than aged-matched subjects who are negative for human immunodeficiency virus (49,50). The latter study (50) also demonstrated that AIDS patients had a different pattern of gastritis, characterized by greater mononuclear cell responses, fewer lymphoid follicles, and a greater prevalence of intestinal metaplasia. The immune response may also prevent the invasiveness of H. pylori, as suggested by the anecdotal but puzzling observation of invasive H. pylori infection in a patient with AIDS (51).

Treatment

Although H. pylori is sensitive to many antimicrobial drugs in vitro, it is difficult to eradicate from the stomach. This may be ascribed to antibiotic breakdown by gastric acid, clearance by gastric emptying, and the difficult-to-penetrate mucous layer in which the bacterium resides. Resistance of H. pylori to specific antibiotics, especially metronidazole, is also frequent. Therefore, it is generally accepted that a combination of at least two, and possibly three, antimicrobial agents should be given for a minimum of 1 week. The regimen found to be most effective is the administration of amoxicillin (or tetracycline) plus metronidazole and bismuth subsalicylate 2 to 4 times a day for 2 to 3 weeks (52). The use of one antibiotic associated with an antisecretory agent, such as a histamine H2 receptor antagonist, has given disappointing results. In contrast, the combination of a proton pump inhibitor (H+-K+ ATPase antagonist) with amoxicillin or acid-stable macrolides (clarythromycin or roxithromycin) appears more promising; a number of studies are being conducted to determine the optimal dose, duration, concomitant therapy, and cost-effectiveness of these compounds (53,54). Recently, it was shown that at least a 7-day course of any of these regimens is required to obtain a high (90%) cure rate, but that continuing treatment for more than 10 days does not significantly improve its efficacy. Finally, topical therapy for 1 h was recently tried with excellent results, albeit in only one center at this time (55). This treatment involves a 2-day administration of a mucolytic agent to dissolve the mucous layer and of a proton pump inhibitor. On the third day, a balloon is introduced into the second portion of the duodenum under fluoroscopic control, and a solution of pronase, amoxicillin, metronidazole, and bismuth subsalicylate is injected into the stomach, where it is left for 1 h. The presence of the duodenal balloon appears to prevent emptying of the antibiotics and the mucolytic agent, thus ensuring maximum efficacy of the therapy.

Future Research

The past 12 years have seen extensive progress in research on H. pylori as a cause of chronic active gastritis, duodenal ulcer disease, and gastric cancer. This has been largely due to an unusual collaboration among gastroenterologists, pathologists, molecular geneticists, bacteriologists, and immunologists. However, our understanding of how H. pylori colonizes and causes diseases is far from complete, and it will benefit from studies performed in animal models that can be experimentally infected with H. pylori (56-59). In addition, no easily administered treatment leading to eradication of this bacterium in all patients is yet available, although a better knowledge of its physiology may lead to the development of such a "silver bullet." Studies in animals that are not naturally infected with H. pylori suggest possibilities for vaccines (56,57), and ongoing trials in nonhuman primates are exploring the possibility of immunizing hosts that can be naturally infected with this organism. Although the elimination of peptic ulcer disease and of certain forms of gastric cancer will require extensive and coordinated efforts from public health authorities, this goal now appears to be within the reach of the scientific and medical community.

Acknowledgments

The author thanks Drs. P. Baker and D.E. Berg for their helpful comments and suggestions during the preparation of this review.

Dr. Dubois is professor of medicine and surgery (research), assistant director, Digestive Diseases Division, and chief, Laboratory of Gastrointestinal and Liver Studies, F. Edward Hébert School of Medicine of the Uniformed Services University of the Health Sciences, Bethesda, Maryland. He studies the physiology and pathophysiology of gastric secretion and gastric emptying as well as the role of gastric infection with H. pylori in gastroduodenal diseases.

Address for correspondence: Andre Dubois
Department of Medicine
Uniformed Services University
4301 Jones Bridge Road
Bethesda, MD 20814-4799, USA
Fax: 301-295-3676 or -3557
E-mail: dubois@usuhsb.usuhs.mil.

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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. Rats and mice are common animal hosts for L. ballum. Infection in mice is inapparent and can persist for the animal's lifetime. *Rodents are the only major animal species that can shed leptospires throughout their life-span without clinical manifestations. Active shedding by lab animals can go unrecognized until personnel handling the animals become clinically ill.
TRANSMISSION:
Handling affected animals, contaminating hands, or abrasions with urine, or aerosol exposure during cage cleaning are most common. The organism is often transmitted to humans by the urine of the reservoir host. The organism may also enter through minor skin lesions and probably via the conjunctiva. Many infections have followed bathing or swimming in infected waters.
DISEASE IN ANIMALS:
In cattle, fever and anorexia occur with rapid decline in milk yield and atypical mastitis. Pregnant cows abort with retention of the placenta. Also, mild jaundice and severe anemia occurs with enlarged and friable liver and swollen kidneys. In pigs subclinical infection is common, though it can cause abortion and birth of weak piglets. In dogs and cats, gastroenteritis, jaundice, and nephritis may occur.
DISEASE IN MAN:
Ranges from inapparent infection to severe infection and death. Biphasic Illness a. Weakness, headache, myalgia, malaise, chills, & fever. b. Leukocytosis, painful orchitis (testes not usually enlarged), conjunctival effusion, and rash. Icteric leptospirosis (Weil's syndrome-usually caused by L. icterohaemorrhagiae) is the most severe form of the disease, characterized by impaired renal and hepatic function, abnormal mental status, hypotension, and a 5-10% mortality rate. Signs and symptoms are continuous and not biphasic.
DIAGNOSIS:
Early in the disease, the organism may be identified by darkfield examination of the patient's blood or by culture on a semisolid medium. Culture is difficult and requires several weeks. A rapid diagnosis is made with the DOT-ELISA test. *Leptospires can be recovered only from mature mice even though antibodies can be detected from infected mice of all ages.
TREATMENT:
Penicillins or tetracyclines. Can eliminate L. ballum from a colony (mice) with 1000 gm chlortetracycline HCL/Ton of feed for ten days.
PREVENTION\CONTROL:
Vaccination in cattle, swine, and dogs Avoid swimming in or drinking from potentially contaminated water. Protect workers by providing boots and gloves. Rodent control. Drain wet ground. Doxycycline chemoprophylaxis for persons at high exposure.

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. It is now the most common tick transmitted disease in the USA. Also seen in Europe, England, Soviet Union, China, Japan, Southeast Asia, South Africa, Australia, and Canada.
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. Also found in Dermacentor, Rhipicephalus and Amblyomma and other ticks and biting insects, including mosquitoes, fleas, and biting flies. Because of lack of any proof to the contrary it is generally believed at this time that any potential increased risk to human beings from infected animals is attributable to animals bringing ticks into areas of human habitation rather than any pet transmission. Dogs appear to be at greater risk than humans.
DISEASE IN ANIMALS:
Serologic evidence has been reported in the dog, cat, horse, and ruminants. However, correlation with disease is lacking except in the dog. The dog exhibits the same symptoms as noted below for humans. Expanding skin lesions have been noted in mice and rabbits.
DISEASE IN MAN:
Multisystemic disease which may have chronic sequelae; an annular rash known as erythema chronicum migrans (ECM) develops in 60-80% of patients in the area of the tick bite and is considered pathognomonic. Also flu like symptoms, which resolve in about three weeks. 8-10% of people develop cardiac involvement several weeks later. Manifestations include atrioventricular block, cardiomyopathy, heart failure, myocarditis, and pancarditis. 15% develop neurologic disorders such as facial nerve palsies which usually resolve. Other manifestations include meningitis, cranial neuritis, radiculoneuritis, neuropathy, and encephalopathy. 60% develop the most common sequelae, arthritis. Disease may remain latent with symptoms developing 4 years after seroconversion.
DIAGNOSIS:
Most common test is detecting antibody titers by IFA or ELISA (on blood, CSF or synovial fluid). Culture is definitive but is difficult and requires special media such as Barbour-Stoener-Kelly media. Histologically with Dieterle Silver Stain or immunoperoxidase stains, but is often unrewarding.
TREATMENT:
A positive serology is no grounds for treatment when no clinical signs are present. Borrelia burgdorferi is sensitive to tetracycline and moderately sensitive to penicillin. amoxicillin, ceftriaxone, and imipenem are also highly active.
PREVENTION\CONTROL:
Tick control care when removing ticks or when handling potentially infective materials a vaccine against Lyme Disease tested in hamsters has been found effective. More research is needed but in the future vaccination may be beneficial for those at constant risk of exposure.

 

 

 

Neisseria canis

 

Neisseria canis infection: a case report

Sandie Safton,1 Gavine Cooper,1 Michael Harrison,1 Lynne Wright1 and Paul Walsh2

Abstract

The third case report, which is the first in Australia, of human infection with Neisseria canis is documented. This is the first case report in which the pathogenicity of this organism for humans is unequivocally demonstrated. Commun Dis Intell 1999;23:221.

Introduction

Neisseria canis (N. canis ) was first described by Berger in 1962.1 The bacterium’s normal habitat is the throat of the cat and dog. It is regarded as a true Neisseria with phenotypic properties that allow its recognition as a distinct species.2,3 Only two previous case reports of human infection have been found by the authors.4,5 The first case of human infection with N. canis was published by Hoke and Vedros4 in 1982. This isolate came from a cat bite wound on a child. No other clinical details were described. In 1989 N. canis was reported in a mixed culture that included Pasturella multocida (P. multocida) and Eiknella corrodens from a cat bite wound on the arm of a previously healthy 36 year old woman. The wound was inflamed and the patient was successfully treated with amoxycillin.  P. multocida was regarded as the primary pathogen in this case.5

Clinical Features

The patient, a 50 year old male normally in good health, presented with a purulent wound to the sole of his foot, with surrounding cellulitis. The patient recalled having trod on a dog bone a few days previously. A swab for culture was taken and antibiotics commenced (metronidazole and amoxycillin/clavulanic acid). Seven days later he made a complete recovery apart from some residual induration.

Methods

Laboratory Diagnosis

Standard bacteriologic techniques as outlined in the Manual of Clinical Microbiology 6 were used. The Gram stain showed moderate numbers of polymorphs. A moderate pure growth of a small gram negative coccus was obtained on aerobic blood agar, with the formation of yellowish non-haemolytic, 2 - 4 mm slightly flat topped colonies after 48 hours. It grew well on nutrient agar but did not grow on MacConkey agar. The organism was a facultative anaerobe, non-capnophilic and growth at 37oC was better than at 30oC or 42oC. The remainder of the diagnostic tests were consistent with the identification of N. canis, and it was sensitive to benzylpenicillin, erythromycin, and tetracycline but resistant to vancomycin.

A conserved segment (441 base pairs) of the isolate’s RNA was subject to molecular studies, using BLAST analysis with the GeneBank7 data bank. A significant similarity was found with a sequence of 422 matching base pairs (95%) with GenBank Accession number L06170 - Neisseria canis ATCC 14687.

Discussion

It is considered without doubt that N. canis was pathogenic. Currently the organism is a very rare isolate associated with cat or dog contact, but it may be under reported. The laboratory diagnostic clues are the isolation of an oxidase positive, gram negative, non-fastidious coccus that is very strongly catalase positive and forms dull yellow flat-topped non-haemolytic colonies on Day 2.  It is nitrate positive but otherwise essentially asaccharolytic and rather inert in its biochemical reactions. It is described in the literature as galactosidase negative, tributyrin hydrolysis negative, DN’ase negative, nitrite negative and polysaccharide synthesis negative.3,6 Currently there is no reason to suspect that the organism would not be covered by the current Australian Antibiotic Guidelines8 for the management of animal bites.

References

1. Berger U. Uber das vorkommen von neissien bei einigen. Tieren. Z Hyg. 1962;148:445-57.

2. Weyant RS, et al. Identification of unusual pathogenic gram- negative aerobic and facultatively anaerobic bacteria. 2nd Edition. Baltimore: Williams and Wilkins, 1995.

3. Krieg NR, Hold JG (Eds). Bergey’s manual of systematic bacteriology, Vol 1. Baltimore: Williams and Wilkins, 1984.

4. Hoke C, Vedros NA. Characterizat