Infectious Disease Flashcards

Question

Mycobacterial infections: commonly seen in dogs and cats?

Answer 1

Mycobacterial infections are rare in both cats and dogs. However, more cases are seen in cats; the majority of which present as skin lesions. These are typically seen as cutaneous nodules, draining tracts, and/or ulceration. In some cases, the disease may become generalized secondary to skin inoculation, but only occasional cases present with primary systemic disease. The current epidemiology of tuberculosis in cats is unclear. Two main theories currently exist; (1) indirect spread from cattle and/or badgers or (2) direct spread from wild rodents and other small mammals.

Answer 2

Dogs and cats are spillover hosts and as such are believed to present a low risk of further dissemination, either to humans or other animals. However, all members of the tuberculosis complex pose potential zoonotic risks.

Answer 3

MAC organisms are ubiquitous saprophytes to which humans and animals are extensively exposed. However, MAC infections rarely cause disease as many mammals, including cats and dogs, are believed to be innately resistant. That said, occasional infections have been seen in pigs, deer, horses, cats, dogs, and humans. Dogs are believed to be more susceptible to M. tuberculosis and M. bovis than cats, but relatively resistant to MAC infections. Many cases of feline and canine tuberculosis may be subclinical in nature. Infection usually occurs after protracted exposure (e.g., repeated exposure to infected small mammals, living on a farm housing tuberculous cattle, or living for prolonged periods with infected humans or poultry). Tuberculosis is therefore seen mainly in adult animals

Answer 4

Depending on the route of infection, affected cats and dogs may present with systemic signs related to the alimentary and/or respiratory tracts or with localized disease affecting the skin (which may later develop pulmonary involvement). Historically, cats most commonly developed alimentary lesions (secondary to being infected by drinking tuberculous milk) while dogs developed pulmonary lesions (secondary to inhaling infected droplets of their owner's sputum) . However, the most usual presentation for tuberculosis in cats is now the cutaneous form, with respiratory and alimentary forms being seen less frequently

Answer 5

In cats, MAC has been associated with cutaneous lesions, otitis externa with peripheral vestibular disease, generalized lymph node and pulmonary involvement, pulmonary and gastrointestinal disease, intracranial-space occupying granuloma,[and disseminated tuberculosis. Disease caused by MAC appears to be more likely to cause systemic disease than M. bovis or M. microti In dogs, MAC has most commonly been reported to cause disseminated tuberculosis, typically involving the lymph nodes, liver, spleen, and intestines.

Answer 6

M. lepraemurium Bite wounds Feline leprosy is primarily a cutaneous syndrome.

Answer 7

Canine leproid granuloma syndrome (CLGS) is similar to feline leprosy, with affected dogs developing granulomas of the skin and subcutis, which contain variable numbers of acid-fast bacilli that generally do not grow using standard mycobacterial culture methods.

Answer 8

Infection with NTM can produce a number of different clinical syndromes. The most common syndromes in cats are (1) granulomatous panniculitis and (2) single or multiple cutaneous or subcutaneous nodules, but (3) disseminated disease can also be seen. Interestingly, some organisms (e.g., M. fortuitum) can cause all three syndromes. “Bite site” lesions

Answer 9

Four of the six species of Brucella (B. canis, abortus, melitensis, and suis, excluding ovis and neotomae) can infect dogs. Exposure to B. abortus occurs by ingestion of aborted or fetal tissue from diseased livestock.

Answer 10

Brucella canis enter the dog's body through ingestion, licking, breeding, or contact with exposed mucous membranes of the eye, mouth, nose, vagina, and penis. B, Brucella canis attach to the exposed mucous membranes, are engulfed by mononuclear phagocytes, and enter the lymphatic drainage to later gain access to the dog's bloodstream. C, The bacteria become sequestered in the nearest regional lymph nodes, where replication causes enlargement or lymphadenopathy for subsequent seeding of steroid-dependent tissues, vertebrae, and eyes. D, Brucella canis inflame the female and male reproductive organs, respectively. These intracellular organisms inhabit the vaginal vault and uterus, which promotes spread by coital contact during natural breeding, early embryonic death, abortion and stillbirth, or whelping of bacteremic pups. Inflammation of the epididymis, testis, and prostate provide bacterial shedding in semen, altered spermatogenesis, increased abnormal sperm morphology, testicular degeneration, and atrophy with eventual infertility of male and female dogs.

Answer 11

In males, the prostate, testicle, and epididymides produce a continuous or recurrent release of bacteria in venereal secretions for months to years. These organs serve as effective sites for widespread dissemination to males if actively breeding. Urine becomes a contaminated vehicle by the close anatomic connection of the bladder to the secretory prostate and epididymis. Prostatic fluid moves cranially into the bladder by normal urethral pressure. In the female, the gravid uterus, fetus, and placenta are targeted. Bacteria are found in fetal stomach contents, suggesting that a fetus may swallow infected amniotic fluid in uterus. An aborting bitch is of high risk for the spread within any environment. The blood-borne bacteremia can infect intervertebral disks, the kidney, and anterior uvea of the eye. Time from initial exposure to bacteremia is 3 weeks

Answer 12

Despite an ongoing systemic infection, clinical signs can range from none, to mild, to severe reproductive dysfunction. No clinical sign is pathognomonic for canine brucellosis, but the disease should always be given primary consideration in dogs examined for reproductive failure or infertility. Infected dogs are not seriously ill. Fever is uncommon because this bacterium lacks the lipopolysaccharides found in other Brucella strains that produce endotoxins. B. canis targets androgen-dependent organs in the male (i.e., epididymis, prostate). An intact infected stud dog may exhibit epididymitis, orchitis, a painful scrotal enlargement, preputial discharge, or testicular atrophy Clinical signs in the bitch include infertility, apparent failure to conceive, early embryonic death (EED), fetal resorption, or failure to whelp. Some pups die within hours of birth. Surviving pups are usually bacteremic for a minimum of several months. Some males have an absence of sperm. Either gender may develop discospondylitis, uveitis, or meningoencephalitis.

Answer 13

A positive blood culture is definitive proof of infection. Serologic testing is more accurate in proestrus or during estrus since the bacteremia is elevated under hormonal influence.

Answer 14

Antimicrobial therapy is not encouraging. Since B. canis is sequestered inside cells for extended periods and the bacteremia is episodic, single antibiotic regimens are less successful. Relief has come from the combination of tetracyclines (tetracycline HCl, chlortetracycline, doxycycline, minocycline) and dihydrostreptomycin. Antibiotics lower the bacteremia and thus give a false interpretation for any negative serologic result.

Answer 15

A potent neurotoxin produced by the bacterium Clostridium tetani. C. tetani is a motile, gram-positive, nonencapsulated, anaerobic, spore-forming, rod-shaped bacterium. All toxigenic strains produce two toxins, a tetanus neurotoxin (tetanospasmin) and a hemolysin (tetanolysin), the latter with no clinical relevance.

Answer 16

Tetanus develops if C. tetani spores enter wounds and anaerobic conditions favor germination and toxin production. The H-chain of tetanospasmin has a high affinity to ganglioside surface receptors on neuromuscular endplates. It is responsible for internalization, cytosolic translocation, and fast retrograde axonal transport of the L-chain. The L-chain represents the actual neurotoxin. Within the spinal cord and brainstem, the neurotoxic L-chain spreads transsynaptically to inhibitory interneurons (Renshaw cells) of motor and autonomic centers. The general clinical picture of tetanus is the consequence of loss of inhibition of α-motoneuron firing. Mild stimuli will cause severe unopposed contractions of extensor muscles. Similarly, autonomic control may be lost and increased sympathetic or parasympathetic activity will occur.

Answer 17

Younger dogs are more susceptible. Tetanus can present as a generalized syndrome or as localized tetanus.

Answer 18

In localized tetanus, the toxin enters the motor axon closest to the injury site and migrates by retrograde transport to the neuronal cell bodies within the spinal cord or brainstem, where it exhibits its action. Animals with localized tetanus frequently have stiffness in one limb or muscle group close to the injury site. Stiffness usually progresses to the point that the limb is held in rigid extension

Answer 19

Localized tetanus can be distinguished from severe upper motor neuron (UMN) monoparesis by the ability to initiate postural reactions despite muscle stiffness in more mild cases and by the inability to passively flex the limb in severe cases. (Localized tetanus with involvement of either both pelvic or thoracic limbs has been reported)

Answer 20

Dogs and cats affected with generalized tetanus have generalized muscle stiffness of variable intensity, hypersensitivity to touch, lights, and sounds, but a normal mental state. Most dogs will show characteristic facial muscle spasms: wrinkling of the forehead, erect ears that are drawn together, lips that are drawn back (risus sardonicus), and protrusion of the third eyelid from enophthalmus due to continuous or episodic contraction of extra ocular muscles. Trismus (lockjaw) caused by contraction of masticatory muscles, salivation, laryngeal spasms, and dysphagia may occur. Mildly affected dogs are still ambulatory, but show a stiff gait. Postural reactions are initiated, but performance is stiff. Patellar reflexes are often exaggerated, but flexor reflexes may appear decreased with increasing muscle stiffness. Severe hyperthermia (>104° F) due to muscular spasms is often present.

Answer 21

Seizures may develop in severely affected animals. Dysphagia and laryngeal spasms, which may cause severe respiratory impairment, are common. Transient megaesophagus and hiatal hernia from esophageal dysfunction may cause regurgitation and aspiration pneumonia. Dogs may be unable to urinate due to urethral spasms and require placement of an indwelling catheters. Some dogs may be constipated. Autonomic dysfunction may also occur in dogs. Severe bradyarrhythmias may require temporary pacemaker placement

Answer 22

Class I: normal gait, hypersensitivity to noise, light, or touch) Class II: stiff gait Class III: recumbent dogs with tonic muscle contractions, fasciculations, spasms or seizurestypical head involvement Class IV: dogs with autonomic signs independent of ambulatory status. The survival rate decreases with the severity class.

Answer 23

Tetanus antitoxin should be administered to neutralize any toxin that is unbound or yet to be formed but does little to hasten recovery. Recovery in most cases is slow, progressive, and based on sprouting of new nerve terminals. Therapy should be administered in an attempt to kill any existing vegetative C. tetani organisms. Metronidazole and penicillin G are the drugs of choice for treatment of tetanus. Clindamycin and tetracycline are also effective

Answer 24

Neuronal uptake and action of the neurotoxin is irreversible, and recovery requires the outgrowth of new nerve terminals, which explains the long duration of the disease.

Answer 25

Botulism is a paralytic illness caused by a group of neurotoxins commonly produced by Clostridium botulinum as well as occasionally by other toxigenic clostridia. Botulinum toxins are highly potent. The toxins inhibit acetylcholine release at peripheral cholinergic synapses, which results in generalized lower motor neuron (LMN) and autonomic dysfunction.

Answer 26

Clostridium botulinum represents a group of gram-positive, spore-forming, anaerobic saprophytic, rod-shaped bacteria with worldwide distribution which are distinguished by their specific neurotoxins. Seven different types of botulinum toxins are currently recognized: Up to now, botulinum toxin type C has been identified as causative agent in the majority of cases.

Answer 27

Clostridial spores and organisms are present in the environment in soil and water if organic material is provided. Spores are highly resistant to dry heat, light, drying, and radiation. the intestinal tract. In the intestinal environment; an alkaline pH permits its dissociation. its dissociation. The most common mode of intoxication in people and animals is ingestion of the preformed toxin (food-borne botulism). Most cases in dogs are associated with the ingestion of carrion. Cadavers of birds are frequent sources of intoxication,[6-11] because their intestines often contain C. botulinum type C.

Answer 28

With food-borne botulism, botulinum toxin is absorbed from the upper small bowel into the lymphatic system and thereafter distributed hematogenously to axon terminals of cholinergic nerves. Botulinum toxin does not cross the blood-brain barrier. The H chain is responsible for the specific binding to a high-affinity surface receptor complex on the surface of the nerve, internalization of the toxin (receptor-mediated endocytosis), and translocation into the cytosol of the peripheral nerve.

Answer 29

The L-chain represents the actual neurotoxin at the neuromuscular endplate. It acts as a zinc-dependent endopeptidase that cleaves and thus inactivates SNARE proteins; thereby mediating docking and fusion of neurotransmitter vesicles to the presynaptic plasma membrane and thus promote calcium-mediated neurotransmitter release into the synaptic cleft. All toxin types block acetylcholine release at the neuromuscular endplate resulting in generalized LMN dysfunction.

Answer 30

Botulism has an acute onset. The incubation period can range from hours to 6 days but, in most cases, clinical signs will develop rather soon (1 to 3 days) after ingestion of contaminated food. Course and severity of illness vary in direct proportion to amount of ingested toxin. Severely affected dogs may progress to flaccid tetraplegia in less than 24 hours, while others may show only weakness in the hind limbs, forelimbs, and the muscles of the neck and head. Cranial nerve signs are common in severely affected animals. Neurologic examination indicates generalized LMN disease. Muscle tone is reduced and spinal reflexes (patellar, withdrawal) are absent. In animals that are not yet completely tetraplegic, postural reactions demonstrate preserved ability to sense position and initiate movement (sensory), while performance (motor) is progressively reduced. Mentation is normal, and conscious response to pain stimuli is completely preserved, although the animal may not be able to move its legs or head. More mildly affected animals may not have cranial nerve signs. Reversible megaoesophagus has been described in dogs. Mydriatic pupils, keratoconjunctivitis sicca, constipation, urinary retention, and variable heart rate are signs or parasympathetic dysfunction. Severely affected animals die from respiratory paralysis. Spontaneous recovery will occur if respiratory paralysis can be avoided.

Answer 31

Treatment is mainly supportive, because spontaneous recovery will occur in most dogs within 2 to 3 weeks if the amount of ingested toxin is not too large and respiratory failure and complications like pneumonia or urinary tract infections are avoided. Hypokalemia and any magnesium-containing preparations should be strictly avoided because this additionally impairs neuromuscular function

Answer 32

Bartonella species are gram-negative bacteria that are highly adapted to many mammalian reservoir hosts within which these bacteria can cause a long-lasting intraerythrocytic bacteremia. Colonization of erythrocytes may facilitate efficient vector transmission and potentially contribute to decreased antimicrobial efficacy. Bartonella species are also reported to colonize vascular endothelial cells.

Answer 33

Nonhemolytic intracellular colonization of erythrocytes and endothelial cells would preserve the organisms for efficient vector transmission, protect Bartonella from the host immune response, and potentially contribute to decreased antimicrobial efficacy

Answer 34

Bartonella endocarditis occurs in large-breed dogs with a high predilection for aortic valve involvement. In some dogs, intermittent lameness, bone pain, epistaxis, or fever of unknown origin precede the diagnosis of endocarditis by several months, whereas other dogs will present with an acute history of cardiopulmonary decompensation. Cardiac arrhythmias, secondary to myocarditis, can be detected in dogs lacking echocardiographic evidence of endocarditis. Infection with B. henselae or B. vinsonii subsp. berkhoffii alone or in conjunction with Ehrlichia canis and Leishmania infantum may cause epistaxis in dogs. Based on serologic and molecular evidence, B. vinsonii subsp. berkhoffii, B. henselae, or other Bartonella species appear to contribute to the development of dermatologic lesions indicative of a cutaneous vasculitis, panniculitis, anterior uveitis, polyarthritis, meningoencephalitis, immune-mediated thrombocytopenia (ITP) or immune-mediated hemolytic anemia (IMHA) and splenomegaly in dogs. Although detection of ITP, IMHA, and polyarthritis in conjunction with finding antinuclear antibodies is consistent with a diagnosis of SLE, occult Bartonella infection should be ruled out prior to administration of immunosuppressive drug therapy. These data suggest that Bartonella spp. can induce lymphatic as well as intravascular infection in dogs

Answer 35

To date, an optimal protocol has not been established for the treatment of Bartonella infections in cats, dogs, or people. Regardless of the antibiotic that is used therapeutically, a long duration of antibiotic administration (4 to 6 weeks) may be necessary to eliminate the infection. Macrolides (azithromycin, clarithromycin) most probably represent the oral antibiotic class of choice for treating Bartonella infections. Fluoroquinolones alone, or in combination with amoxicillin, have also elicited a positive therapeutic response in dogs.

Answer 36

Bartonella henselae is believed to be naturally transmitted among cats by cat fleas (Ctenocephalides felis felis). The exact localization of Bartonella in cats has not been completely determined. Bartonellae have been detected within erythrocytes of naturally infected cats and in vitro. Bartonella may also localize within vascular endothelial cells of infected cats as has been suggested for rodents.

Answer 37

Existing data indicate that few cats naturally infected with Bartonella have clinical signs. Some cats developed fever following elective surgical procedures. Uveitis may be a manifestation of natural Bartonella infection. Bartonella henselae type I was associated with fatal blood culture–negative vegetative aortic valve endocarditis in a naturally infected cat.

Answer 38

Documenting clearance of Bartonella infections through antibiotic treatment is difficult due to the prolonged relapsing bacteremia of most infected cats. No regimen of antibiotic treatment has been proven effective, in controlled studies with long-term follow-up, for definitively eliminating Bartonella infections in cats. Routine treatment with antibiotics may induce resistant strains; therefore, treatment should be reserved for use only in Bartonella-positive cats showing clinical signs. Although treatment reportedly decreases the level of bacteremia in cats, there is no concrete evidence that treatment of the cat will decrease the probability of transmission of Bartonella infection to an owner.

Answer 39

Gram negative. Organisms from the genus Ehrlichia are grouped within the family Anaplasmataceae. Also within this family are the bacteria Anaplasma platys and Anaplasma phagocytophilum, which cause canine thrombocytic and granulocytic anaplasmosis, respectively, and organisms belonging to the genera Neorickettsia, which includes Neorickettsia risticii and the agent of salmon poisoning disease (SPD), Neorickettsia helminthoeca. (The families Rickettsiaceae and Anaplasmataceae are phylogenetically related through the order Rickettsiales)

Answer 40

These organisms are transmitted to dogs and cats by arthropod or trematode vectors, and many are maintained in nature through infection of wild animal reservoir hosts. They also have the potential to be transmitted by blood transfusion. Their geographic distribution is generally restricted to that of their vectors and intermediate hosts.

Answer 41

Ehrlichia canis is the cause of canine monocytic ehrlichiosis (CME) Replication of the organism in reticuloendothelial tissues is associated with generalized lymphadenopathy and splenomegaly. Ocular and nasal discharges, peripheral edema, and less commonly, petechial and ecchymotic hemorrhages may also occur. Neurologic signs, including twitching, ataxia, seizures, vestibular signs, hyperesthesia, and cranial nerve defects, may occur as a result of meningeal inflammation or hemorrhage. Thrombocytopenia and sometimes mild leukopenia and anemia occur 1 to 4 weeks after infection. Acute signs generally resolve after 2 to 4 weeks, after which dogs may remain subclinically infected. Mild thrombocytopenia may persist during this phase.

Answer 42

Sequestration of organisms within the spleen may occur, and the organisms may evade the host immune system through antigenic variation. This phase may persist for months to years. Bleeding tendencies result from thrombocytopenia and platelet dysfunction. The finding of pancytopenia within the complete blood count (CBC) typifies the severe chronic form of ehrlichiosis, and results from hypoplasia of all bone marrow cells. More commonly, a nonregenerative anemia and thrombocytopenia are noted, although these are not always present.

Answer 43

Moderate to marked granular lymphocytosis (up to 17,000/µL) and bone marrow plasmacytosis may occur, sometimes accompanied by a monoclonal gammopathy, which may lead to misdiagnosis of lymphocytic leukemia or multiple myeloma, respectively. This has led to the recommendation that all dogs with well-differentiated lymphocytosis or otherwise unexplained monoclonal gammopathy be tested for E. canis infection

Answer 44

Serum chemistry abnormalities in chronic ehrlichiosis include hypoalbuminemia, hyperglobulinemia, and elevated alanine aminotransferase and alkaline phosphatase activities. Most often the hyperglobulinemia is due to a polyclonal gammopathy. Less commonly, elevations in blood urea nitrogen and creatinine may be noted. A protein-losing nephropathy may develop as a result of an immune-complex glomerulonephritis.

Answer 45

The finding of morulae within monocytes using cytologic evaluation is diagnostic for monocytic ehrlichiosis, but is insensitive. More commonly, the diagnosis of ehrlichiosis is made using serology, which may be performed using indirect fluorescent antibody (IFA) testing, enzyme-linked immunosorbent assay (ELISA) technology, or Western blotting. Testing for E. canis DNA using the polymerase chain reaction (PCR) is likely to be more sensitive than IFA or ELISA in dogs with acute disease. Blood culture can be performed as well. The treatment of choice for CME is doxycycline

Answer 46

Within granulocytes. Dogs show signs of fever, lethargy, anorexia, and neutrophilic polyarthritis, neurological signs.

Answer 47

A. phagocytophilum forms morulae in granulocytes, most commonly neutrophils. A. phagocytophilum is spread by several Ixodid tick species, and is transmitted only transstadially within the tick. The tick must attach for 24 to 48 hours before transmission can occur. Because Borrelia burgdorferi is transmitted by the same Ixodid ticks, coinfections with B. burgdorferi and A. phagocytophilum are frequently detected, and the two may enhance one another's pathogenicity.

Answer 48

Include fever, depression, inappetence, and scleral injection, and occur after an incubation period of 1 to 2 weeks. Mild lymphadenomegaly and splenomegaly may occur. Neutrophilic polyarthritis has been detected in a few dogs. neurologic disease. Laboratory abnormalities include thrombocytopenia, which is present in over 80% of cases, lymphopenia, eosinopenia, and a mild nonregenerative anemia. The serum chemistry panel may reveal hypoalbuminemia and mild to moderately elevated liver enzymes. Infection with A. phagocytophilum appears to be immunosuppressive. The organism survives within neutrophils by inhibiting phagosome-lysosome fusion, suppression of the respiratory burst, and through inhibition of neutrophil apoptosis. As a result, dogs infected with A. phagocytophilum may be prone to other infections, particularly bacterial infections

Answer 49

The finding of morulae within neutrophils in an endemic area is highly suggestive of infection with A. phagocytophilum, although the morulae cannot be distinguished from those of E. ewingii. Morulae, when present, are found in 7% to 37% of circulating neutrophils. Diagnosis can also be accomplished using acute and convalescent phase serology. Determination of the infecting species can be accomplished using PCR. The organism can also be cultured from blood in HL-60 cell culture. Treatment: doxycycline

Answer 50

Anaplasma platys is the cause of canine thrombocytic anaplasmosis. This organism forms morulae within platelets, and is yet to be cultured. The vector of A. platys is unknown. Thrombocytopenia occurs at 1 to 2 week intervals. Because of cross-reactions with A. phagocytophilum, serology is not diagnostic for A. platys infection. A. platys–specific PCR assays have also been developed. Use of splenic or bone marrow aspirates for PCR should be considered when blood samples test negative. Treatment of canine thrombocytic anaplasmosis is as for granulocytic anaplasmosis.

Answer 51

Neorickettsia helminthoeca causes SPD. SPD has geographic distribution that is restricted to the western slopes of the Cascade Mountains from northern California to the Canadian border, with cases also being reported from southern Vancouver Island. Disease may occur elsewhere following transportation of infected fish for feeding at a remote location, or in dogs that travel to and from a nonendemic area to a site containing infected fish. The vector of SPD is a fluke that harbors the organism throughout its life cycle. Fluke eggs transform into miracidia, which infect a small snail, which inhabits fresh or brackish stream water. Cercariae leave the snail and penetrate a fish, most commonly a salmonid fish. Dogs become infected with the rickettsia after ingesting parasitized fish, after which the metacercariae transform into adult flukes. Cats are not susceptible to SPD. After maturation and attachment to the intestinal tract, the fluke somehow inoculates the rickettsia into the host. Subsequently, N. helminthoeca infects and replicates within cells of the mononuclear-phagocyte system. Rapid dissemination of the organism to the lymph nodes, spleen, liver, lungs, and brain occurs. the earliest clinical signs are usually fever, which may be severe, and anorexia. This may be followed by depression, weight loss, lymphadenopathy, vomiting, and diarrhea, sometimes containing blood

Answer 52

Rickettsia rickettsii, the cause of RMSF, belongs to the Rickettsiaceae. Tick-borne rickettsiae cause disease by infecting vascular endothelial cells and increasing microvascular permeability, possibly through generation of reactive oxygen species and lipid peroxidation. The organisms inhibit apoptosis, favoring rickettsial growth. Widespread endothelial injury is associated with production of proinflammatory cytokines and activation of the coagulation cascade, in the absence of disseminated intravascular coagulation.

Answer 53

RMSF is a severe, life-threatening rickettsial illness of humans and dogs caused by Rickettsia rickettsii. Although originally reported from the Rocky Mountain states, RMSF most commonly occurs in the south-central, southeastern, and south Atlantic states of the United States. It is one of the most important emerging diseases in the United States, as well as Central and parts of South America. The organism is transmitted within the tick. Dogs may develop edema and erythema of extremities, including the lips, muzzle, scrotum, penile sheath, pinnae and, rarely the ventral abdomen. Stiffness and reluctance to walk. involvement of muscles, joints, or meninges. Ocular manifestations are common. Petechial and ecchymotic hemorrhages. Neurologic sig. pulmonary edema, cardiac arrhythmias due to myocarditis, hepatomegaly, icterus.

Answer 54

Multiple pathogenic protozoans infect dogs and cats. The group can be divided into amoeba, ciliates, coccidians, flagellates, Microspora, and Piroplasmia. Protozoans generally cause either gastrointestinal (GI) tract disease (enteric protozoans) or polysystemic disease

Answer 55

• The flagellates, Giardia spp., Tritrichomonas foetus, and Pentatrichomonas hominis • The coccidians, Besnoitia spp., Cryptosporidium spp., Cyclospora cayetanensis, Cystoisospora spp., Hammondia spp., Neospora caninum, Sarcocystis spp., and Toxoplasma gondii; • The ciliate, Balantidium coli • The amoeba, Entamoeba histolytica.

Answer 56

fecal oral transmission occurs with the enteric protozoans. The coccidians produce oocysts. Cryptosporidium spp. oocysts are immediately infectious when passed by the host; T. gondii, N. caninum, and Cystoisospora spp. must sporulate outside the host to be infectious (

Answer 57

In the flagellate group, both trophozoites and cysts of Giardia spp. are potentially infectious; however, transmission occurs most frequently after ingestion of cysts because gastric secretions generally kill trophozoites.

Answer 58

Carnivorism can result in infection by other enteric protozoans like Cryptosporidium spp., Giardia spp., E. histolytica, and B. coli if the organisms are present in the intestines of the prey species.

Answer 59

After tissue cyst ingestion, infected cats rarely shed oocysts of T. gondii for more than 2 weeks. For the other enteric protozoans, fecal shedding can be of longer duration. For example, cats infected with T. foetus or Cryptosporidium spp. can shed the organisms continuously or intermittently for months.

Answer 60

Cystoisospora spp. and T. gondii replicate in intestinal cells and may result in clinical illness from cell destruction. Tissue invasion also can occur with E. histolytic. Giardia spp. and Cryptosporidium spp. are found on the surface of enterocytes, so pathogenesis is unlikely secondary to direct cell damage. Some of the pathogenic mechanisms proposed for these enteric agents include production of toxins, disruption of normal flora, induction of inflammatory bowel disease (IBD), inhibition of normal enterocyte enzymatic function, blunting of microvilli, and induction of motility disorders.

Answer 61

Clinical illness associated with T. gondii, N. caninum, and S. neurona generally results from the tissue phase of the infections. Giardia spp. and Cryptosporidium spp. infections are common in young animals, but GI signs can occur in animals of any age. Clinical disease is more common, and duration of organism shedding into the environment may be prolonged in dogs and cats with immunodeficiency-inducing concurrent diseases. Owner concerns in dogs or cats with enteric protozoal infections generally are vomiting, inappetence, or diarrhea; fever is uncommon. Giardia spp., Cryptosporidium spp., and T. gondii infections are most commonly associated with small-bowel diarrhea; E. histolytica, B. coli, and T. foetus infections are most commonly associated with large-bowel diarrhea. Cystoisospora spp. infections can cause clinical signs of large- or small-bowel diarrhea.

Answer 62

Documentation of oocysts, trophozoites, or cysts on direct fecal examination or fecal flotation. Thus animals with enteric protozoal infections that do not respond to therapy should be evaluated for underlying causes of disease. Giardia spp., Cryptosporidium spp., Cystoisospora spp., and Sarcocystis spp. are commonly found in animals with normal stools.

Answer 63

Giardia spp. infections of dogs and cats generally respond clinically to the administration of metronidazole, fenbendazole, or febantel-pyrantel-praziquantel, but infection is usually not eliminated. Metronidazole also helps correct the anaerobic bacterial overgrowth or Clostridium perfringens overgrowth that commonly accompanies giardiasis. In addition, metronidazole may also be beneficial due to inhibition of lymphocyte function.

Answer 64

The coccidians Hepatozoon americanum, Neospora caninum, and Toxoplasma gondii, the flagellates Leishmania spp. and Trypanosoma cruzi, and the piroplasms Cytauxzoon felis and Babesia spp

Answer 65

Results from pyogranulomatous inflammation; glomerulonephritis or amyloidosis may occur secondary to chronic inflammation and immune complex disease. H. americanum has resulted in illness in all age groups, but disease is most commonly recognized in puppies. Fever, weight loss, and severe hyperesthesia over the paraspinal regions are common findings. Anorexia, pale mucous membranes from anemia, depression, oculonasal discharge, and bloody diarrhea occur in some dogs. Clinical signs can be intermittent and recurrent.

Answer 66

Neospora caninum is a coccidian previously confused with T. gondii due to similar morphology. The sexual cycle is completed in the GI tract of dogs and results in the passage of oocysts in feces. Sporozoites develop in oocysts within 24 hours of passage. Tachyzoites (rapidly dividing stage) and tissue cysts containing hundreds of bradyzoites (slowly dividing stage) are the other two life stages. Infection has been documented after ingestion of infected bovine placental tissue and tissue from naturally infected deer. Transplacental infection has been well documented; dams that give birth to infected offspring can repeat transplacental infection during subsequent pregnancies

Answer 67

Although organism replication occurs in many tissues, clinical illness primarily reflects neuromuscular infection in dogs. A number of clinical syndromes associated with neosporosis have been reported in dogs. Congenitally infected puppies develop ascending paralysis with hyperextension of the hindlimbs; muscle atrophy occurs in many cases. Polymyositis and multifocal CNS disease can occur alone or in combination. Clinical signs can be evident soon after birth or may be delayed for several weeks. Neonatal death is common. Although disease tends to be most severe in congenitally infected puppies, dogs as old as 15 years have been clinically affected. In some dogs, myocarditis, dysphagia, ulcerative dermatitis, pneumonia, and hepatitis occur. If not treated, most affected dogs die. (Encephalomyelitis and myositis develop in experimentally infected kittens and some naturally exposed cats are seropositive for N. caninum antibodies, but clinical disease in naturally infected cats has not been reported). No specific hematologic or biochemical findings exist.

Answer 68

Toxoplasma gondii is one of the most prevalent parasites infecting warm-blooded vertebrates. Only cats complete the coccidian life cycle and pass environmentally resistant oocysts in feces. Dogs can pass oocysts in feces after the ingestion of feline feces. 2. Sporozoites develop in oocysts after 1 to 5 days of exposure to oxygen and appropriate environmental temperature and humidity. 3. Tachyzoites disseminate in blood or lymph during active infection and replicate intracellularly rapidly until the cell is destroyed. 4. Bradyzoites are the slowly dividing, persistent, tissue stage that form in the extraintestinal tissues of infected hosts as immune responses attenuate tachyzoite replication. 5. Tissue cysts form readily in the CNS, muscles, and visceral organs. Infection of warm-blooded vertebrates occurs after ingestion of any of the three life stages of the organism or transplacentally. Most cats are not coprophagic and are usually infected by ingesting T. gondii bradyzoites during carnivorous feeding; oocysts are shed in feces from 3 to 21 days. Sporulated oocysts can survive in the environment for months to years and are resistant to most disinfectants. Bradyzoites may persist in tissues for the life of the host. Approximately 30% to 40% of cats and 20% of the dogs in the United States are seropositive and therefore presumed to be infected

Answer 69

Death in dogs and cats that develop overwhelming intracellular replication of tachyzoites after primary infection; hepatic, pulmonary, CNS, and pancreatic tissues are commonly involved. Immune deficiency secondary to viral infection or immune suppressive therapy can also induce fatal toxoplasmosis. Common clinical findings in cats with disseminated toxoplasmosis include depression, anorexia, fever followed by hypothermia, peritoneal effusion, icterus, and dyspnea.

Answer 70

Chronic toxoplasmosis occurs in some dogs and cats. Toxoplasma gondii infection should be on the differential diagnoses list for cats with anterior or posterior uveitis, fever, muscle hyperesthesia, weight loss, anorexia, seizures, ataxia, icterus, diarrhea, cutaneous disease, and pancreatitis. In dogs, respiratory, GI, or neuromuscular infection resulting in fever, vomiting, diarrhea, dyspnea, cutaneous disease, and icterus are most common and occur most frequently in immune-suppressed dogs, such as those with canine distemper virus (CDV) infection or those receiving cyclosporine to prevent rejection of a transplanted kidney. Neurologic signs are dependent on the location of the primary lesions and include ataxia, seizures, tremors, cranial nerve deficits, paresis, and paralysis. Dogs with myositis have weakness, stiff gait, or muscle wasting. Rapid progression to tetraparesis and paralysis with lower motor neuron dysfunction can occur. Some dogs with suspected neuromuscular toxoplasmosis probably had neosporosis. Myocardial infection resulting in ventricular arrhythmias occurs in some infected dogs. Dyspnea, vomiting, or diarrhea can occur in dogs with polysystemic disease. Retinitis, anterior uveitis, iridocyclitis, and optic neuritis occur in some dogs with toxoplasmosis but are less common than in the cat.

Answer 71

To prevent toxoplasmosis, eating undercooked meats or ingesting sporulated oocysts should be avoided. • Cats generally shed oocysts only for days to several weeks after primary inoculation. Most seropositive cats have completed the oocyst shedding period and are unlikely to repeat shedding; most seronegative cats would shed the organism if infected. If owners are concerned that they may have toxoplasmosis, they should see their doctor for testing. Avoiding sporulated oocysts and tissue cysts in undercooked meat can lessen the risk of acquiring toxoplasmosis.

Answer 72

Leishmania spp. are flagellates that cause cutaneous, mucocutaneous, and visceral diseases in dogs, humans, and other mammals. Rodents and dogs are primary reservoirs of Leishmania spp.; people are incidental hosts. Transmission appears to be primarily from dog to dog in Foxhounds in the United States, but transmission by shared needles, blood transfusions, breeding, and congenital transmission can occur. In other countries, the sandfly is the primary vector. Flagellated promastigotes develop in the sandfly and are injected into the vertebrate host when the sandfly feeds. Promastigotes are engulfed by macrophages and disseminate through the body. After an incubation period of 1 month to 7 years, amastigotes (nonflagellate) form and cutaneous lesions develop; sandflies are infected during feeding.

Answer 73

The intracellular organism induces extreme immune responses; polyclonal gammopathies (and occasionally monoclonal), proliferation of macrophages, histiocytes, and lymphocytes in lymphoreticular organs and immune complex formation resulting in glomerulonephritis and polyarthritis are common in dogs.

Answer 74

Visceral leishmaniasis is most common in dogs. Subclinical infection may persist for months or years. When clinical signs occur, weight loss, normal to increased appetite, polyuria, polydipsia, muscle wasting, depression, vomiting, diarrhea, cough, epistaxis, sneezing, and melena are common presenting complaints. Splenomegaly, lymphadenopathy, facial alopecia, fever, rhinitis, dermatitis, increased lung sounds, icterus, swollen painful joints, uveitis, and conjunctivitis are commonly identified on physical examination. Cutaneous lesions are characterized by hyperkeratosis, scaling, thickening, mucocutaneous ulcers, and intradermal nodules on the muzzle, pinnae, ears, and footpads. Many treated dogs respond clinically, but Leishmania cannot be eliminated from the body with drugs. Avoidance of infected sandflies is the only means of prevention

Answer 75

Hyperglobulinemia Hypoalbuminemia Proteinuria Increased liver enzyme activities, t Thrombocytopenia, azotemia, lymphopenia, and leukocytosis with left shift are common in dogs. Hyperglobulinemia is usually polyclonal, but an IgG monoclonal gammopathy was reported in a dog. Leishmania-infected dogs can be positive for antinuclear antibodies in serum, which may lead to the erroneous diagnosis of primary immune-mediated disease.

Answer 76

In some infected dogs, the intracellular replication in red blood cells (RBCs) results intravascular hemolytic anemia. Immune-mediated reactions against the parasite or altered self-antigens worsen the hemolytic anemia and commonly result in positive Coombs' test.

Answer 77

Fever, pale mucous membranes, tachycardia, tachypnea, depression, anorexia, and weakness. Icterus, petechiation, azotemia, and hepatosplenomegaly are present in some dogs depending on the stage of infection and the presence of disseminated intravascular coagulation (DIC). Administration of glucocorticoids or splenectomy may activate chronic disease. Common laboratory abnormalities include regenerative anemia, hyperbilirubinemia, bilirubinuria, hemoglobinuria, thrombocytopenia, metabolic acidosis, azotemia, polyclonal gammopathy, and renal casts. A presumptive diagnosis of clinical babesiosis can be based on historical findings, physical examination findings, test results, and positive serology

Answer 78

Clostridium perfringens, Clostridium difficile, Campylobacter spp., Salmonella spp., and Escherichia coli. (C. difficile, Campylobacter spp., and Salmonella spp. are zoonotic)

Answer 79

C. perfringens is an anaerobic, spore-forming, gram-positive bacillus that has been associated with outbreaks of acute, often severe diarrhea in humans, horses, dogs, and cats. The elaboration of four major toxins (α, β, ι, and ϵ) is the basis for typing the organism into five toxigenic phenotypes, A-E. Each type may also express a subset of at least 10 other established toxins, including C. perfringens enterotoxin (CPE), a well-characterized virulence factor whose production is coregulated with sporulation. Dogs with C. perfringens–associated diarrhea frequently exhibit large-bowel diarrhea characterized by increased frequency of bowel movements with tenesmus, fecal mucus, and hematochezia; however, clinical signs of enteritis or enterocolitis are also common. A strong association has also been detected between the CPE detected via ELISA and acute hemorrhagic diarrheal syndrome (AHDS).[

Answer 80

CPE is a 35-kDa protein encoded by the cpe gene, whose expression is coregulated with sporulation of the organism. The small CPE complex then interacts with additional host proteins, forming several larger complexes. Recent studies have suggested a ∼155 kDa complex is responsible for the cytotoxic and histopathologic damage which provides CPE access to occludin, causing alterations in tight junction structure and function, leading to paracellular permeability changes that contribute to diarrhea.

Answer 81

C. difficile is a gram-positive, anaerobic spore-forming bacillus. C. difficile has been associated with diarrhea and enterocolitis in foals, adult horses, and dogs. Two toxins, toxin A (TcdA, an enterotoxin) and toxin B (TcdB, a cytotoxin), are thought to be primarily responsible for disease associated with the organism, although other toxins may also play a role. In addition, a small percentage of healthy individuals can carry C. difficile in their intestinal tracts without any signs of disease.

Answer 82

Clinical disease is associated with the growth of toxin-producing strains of C. difficile in the intestinal tract, followed by release of toxins and subsequent development of disease. The main virulence factors involved in the pathogenesis of CDI are TcdA and TcdB.[10] Some C. difficile strains can produce a binary toxin (CDT), although its role is unclear

Answer 83

Supportive therapy should be administered and any antibiotics that are concurrently being administered and that may have predisposed the animal to the development of CDI should be discontinued. Metronidazole drug of choice

Answer 84

Campylobacter spp. are small, microaerophilic, gram-negative, curved, rod-shaped bacteria. Campylobacter species that have been implicated in canine enteric disease include C. jejuni, C. coli, C. helveticus, and C. upsaliensis. C. helveticus and C. upsaliensis are the most common isolates in cats. Fecal shedding of C. jejuni is significantly greater in puppies less than 6 months old during the summer and autumn. The unexposed immune system of the pups may increase the susceptibility to intestinal colonization by C. jejuni. Other enteric pathogens, such as parvovirus, Giardia, or Salmonella may play a synergistic role. The isolation of Campylobacter spp. from a diarrheic animal does not necessarily implicate Campylobacter as a cause.

Answer 85

Campylobacter have a fecal to oral route of transmission either through direct contact with fecal material or with objects contaminated with feces. Various virulence factors are associated with colonization, adhesion, invasion, persistence within the host, and host cell damage. The cause of diarrhea due to Campylobacter infection is poorly understood, and the only exotoxin characterized in Campylobacter is cytolethal distending toxin, or CDT. The toxin consists of three proteins, CdtA, CdtB, and CdtC, all of which are required to cause cellular damage. A neutrophilic inflammatory response in the bowel has been described in association with Campylobacter infection, and active intestinal fluid secretion may be due to Campylobacter products that increase cAMP, prostaglandin E2, and leukotriene B4.

Answer 86

Although diarrhea produced by Campylobacter organisms is usually self-limiting, the zoonotic potential of the organism often necessitates medical therapy. The drugs of choice are the macrolides or fluoroquinolones (enrofloxacin). However, due to the high rate of mutational resistance Campylobacter have to the fluoroquinolones, a resistance that sometimes occurs while animals are being treated, fluoroquinolones are not the drug of choice. The macrolides such as erythromycin or azithromycin are the drugs of choice, despite the associated gastrointestinal side-effects with the former drug. The duration of excretion in infected dogs and cats can be as long as 4 months and infected animals should be quarantined away from children during this period.

Answer 87

Salmonellae are primarily motile, non–spore-forming, gram-negative aerobic bacilli. There are currently over 2000 described serotypes of Salmonella

Answer 88

Salmonella infections begin with the ingestion of organisms in contaminated food or water, followed by invasion of M-cells in the Peyer's patches. Salmonella express several fimbriae that contribute to their ability to adhere to intestinal epithelial cells. Salmonella pathogenicity islands (SPI-1 and SPI-2) encode the genes necessary for the invasion of intestinal epithelial cells, induction of intestinal secretory and inflammatory responses, intracellular replication, and establishment of systemic infection.

Answer 89

Salmonella spp. inject an array of bacterial effector molecules into the host cytoplasm, triggering reorganization of the actin cytoskeleton and resultant membrane ruffling. Internalization of Salmonella occurs within minutes of bacterial contact with the host cell. Invasion is followed by inflammation and the influx of neutrophils and macrophages, with consequent secretory diarrhea. The presence or absence of additional virulence factors plays an important role in determining whether septicemia occurs.

Answer 90

Antibiotic therapy is typically only indicated for animals with evidence of systemic disease, or for immunocompromised animals. Antibiotics reported to be effective against Salmonella include fluoroquinolones, chloramphenicol, trimethoprim-sulfonamide, and amoxicillin.

Answer 91

E. coli is a pleomorphic, gram-negative, non–spore forming bacillus that is a member of the family Enterobacteriaceae. Several distinct pathogenic categories (pathotypes) of diarrheagenic E. coli are recognized. Although the virulence determinants of each E. coli pathotype are distinct, they can generally be categorized as either colonization factors (adhesins), which enable the bacteria to bind closely to the intestinal mucosa and resist removal by peristalsis, or secreted toxins, which interfere with the normal physiologic process of host cells.

Answer 92

Despite the occurrence of E. coli as a normal commensal organism in canine intestine, there is increasing evidence that certain E. coli pathotypes cause intestinal infection. The three pathotypes that have been studied in the dog include enterotoxigenic E. coli (ETEC), enterohemorrhagic E. coli (EHEC), and enteropathogenic E. coli (EPEC). Little is known about pathogenic E. coli in cats, although EPEC was isolated from approximately 5% of feline isolates isolated from cats with diarrhea, enteritis, or septicemia.

Answer 93

The incidence of this pathotype in canine diarrhea is unclear. Reported prevalences among diarrheic dogs range from 0% to 31%, particularly in the young.[26] The bacteria colonize the proximal small intestine and produce heat-stable (ST) and occasionally heat-labile (LT) enterotoxins. These enterotoxins result in overproduction of cAMP and cGMP with consequent development of a secretory diarrhea

Answer 94

ENTEROPATHOGENIC E. coli (EPEC) EPEC strains have been associated with diarrhea in a wide range of animal species, including humans. These strains are negative for Shiga-toxin and enterotoxin (ST and LT) genes, but carry the chromosomally located gene, eaeA (E. coli attaching effacing), which facilitates attachment to intestinal epithelial cells and production of the classic “effacing” lesions. E. coli isolates from 44 of 122 dying dogs (36%) with diarrhea were found to have the eaeA gene, and E. coli was the sole pathogen identified in 34%. A close genetic relationship among human, dog, and cat EPEC isolates has been reported, suggesting that EPEC might be transferred between pets and humans.

Answer 95

ENTEROHEMORRHAGIC E. coli (EHEC) Enterohemorrhagic E. coli bind tightly to epithelial cells and produce the same type of attachment-effacement lesions as seen with EPEC. EHEC are minimally invasive but do incite an inflammatory response, predominantly in the large intestine.

Answer 96

The prototype EHEC, a strain of E. coli of the serotype O157:H7, is a significant food-borne human pathogen. Hemolytic-uremic syndrome is the most important complication of E. coli O157 infection, and is characterized by microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure in approximately 7% of human cases. A report documented the isolation of this serotype from dog feces. The isolated strain was found to be identical to a strain isolated from an affected child who had contact with the dog. This finding suggests that similar to cattle, dogs may serve as potential vectors for transmission of EHEC O157. In addition, hemolytic-uremic syndrome has been reported clinically in a small number of dogs.

Answer 97

Clinical signs in infected animals can range from asymptomatic carriage to hemorrhagic diarrhea. In addition, clinical signs can be variable because of the relatively high incidence of concurrent enteric infections with parvovirus, C. perfringens, and intestinal parasites. The predominant clinical sign of enterotoxigenic E. coli infection is profuse watery diarrhea.

Answer 98

The use of antimicrobials is controversial. These bacteria have a relatively high incidence of inherent resistance to antibiotics because of the presence of a .............cell wall and the high incidence of conjugative transfer of .............. determinants. In addition, antibiotic therapy may enhance toxin synthesis or promote its release from the bacteria with a consequent increased rate of hemorrhagic colitis.

Answer 99

This enteropathy has been recently associated with adherent and invasive strains of E. coli, and is typically seen in Boxers less than 4 years of age. There are intriguing similarities between the E. coli strains infecting Boxers and the E. coli LF82 that has been associated with human Crohn's disease. Clinical signs in Boxers include severe and frequent hematochezia with mucus and tenesmus. Administration of fluoroquinolones is associated with rapid resolution of clinical signs and has also been associated with resolution of the cellular infiltration characteristic of this disorder on colonic biopsy. The colonic lesion has also been described infrequently in the French Bulldog and the Border Collie.

Answer 100

1. Clostridium perfringens: There have been no documented cases of zoonotic transmission from dogs or cats to date. 2. Clostridium difficult: The risk of zoonotic transmission is unclear. 3. Campylobacter spp. are potentially zoonotic from dogs to humans with subsequent development of diarrhea. 4. Salmonella spp. Most human Salmonella infections are acquired by handling or consuming contaminated food products, particularly foods of animal origin. Infections also are acquired by direct and indirect contact with farm animals, reptiles, chicks, and occasionally, pets. Infected animals usually shed Salmonella organisms in their feces. Escherichia coli: The potential for zoonotic transmission is unclear; however, some of the strains of pathogenic E. coli found in dogs and cats are indistinguishable from those found in people.

Answer 101

Hemotropic mycoplasmas (hemoplasmas) are small, unculturable epierythrocytic mycoplasmas that are capable of causing severe hemolytic anemia. They infect a wide variety of mammalian species, including man, and have a worldwide distribution. Previously known as Haemobartonella felis, sequence analysis has shown that they fall within the pneumoniae group of mycoplasmas.

Answer 102

Based on visualization of coccoid bacteria associated with erythrocytes on blood smears, and/or the results of specific PCR assays.

Answer 103

Mycoplasma haemofelis, “Candidatus Mycoplasma haemominutum” “Candidatus Mycoplasma turicensis.” Because these organisms cannot be cultured in the laboratory, newly discovered hemoplasmas must be given a Candidatus designation until more information is available to support their classification.

Answer 104

Hemolytic anemia (feline infectious anemia) in immunocompetent cats. Using cytologic evaluation of blood smears, M. haemofelis is pleomorphic, varying from cocci to small rings and rods, sometimes forming short chains of three to six organisms. The results of epidemiologic studies using PCR suggest that this organism is the least prevalent of the three feline hemoplasmas, being found in 0.5% to 5% of sick cats visiting veterinary hospitals.

Answer 105

“Candidatus M. haemominutum” (previously the California strain, or small form of H. felis) is smaller, and has not yet been clearly associated with disease in immune competent cats. (mild anemia in experimentally induced cats). “Candidatus M. turicensis” was first reported in a Swiss cat with severe intravascular hemolysis in 2005.

Answer 106

Until recently, there was only one hemoplasma described that infects dogs, Mycoplasma haemocanis (previously H. canis). This organism usually causes hemolytic anemia in splenectomized dogs, and rarely in dogs with other immunosuppressive disease or concurrent infections.

Answer 107

The mode of transmission for these organisms has been unknown. Fleas and other arthropod vectors may be capable of transmitting infection with M. haemofelis, and transmission of M. haemocanis by the brown dog tick has been demonstrated experimentally. Geographic variation in the prevalence of hemoplasma infection in dogs and cats supports a role for arthropod vectors in transmission.

Answer 108

1. Prebacteremic phase: After inoculation of experimental cats with M. haemofelis, there is a variable delay of 2 to 34 days before acute onset of clinical signs 2. Acute phase: Anemia and bacteremia then occur, and persist for about 18 to 30 days Mortality is highest during this phase. In some cats infected with M. haemofelis, cyclical changes in the hematocrit and numbers of infected erythrocytes occur, with sharp declines in the hematocrit correlating with appearance of large numbers of organisms in blood smears. The number of infected erythrocytes may decline from 90% to <1% in less than 3 hours. Sequestration of organisms in splenic and pulmonary macrophages has been suggested to explain their disappearance. 3. Recovery phase; In surviving cats, the hematocrit then returns to normal or near-normal, and organisms disappear from blood smears. 4. Carrier state; Despite organism disappearance, it has been suggested that recovered cats may remain persistently infected for years , the organism evading the host immune system. Intermittent reappearance of organisms in chronically infected cats, with relapse of anemia, has been documented in some studies. The carrier state being more frequent for “Candidatus M. haemominutum” but less frequent for M. haemofelis.

Answer 109

Depression, inappetence, and dehydration are common signs of infection with M. haemofelis, and some cats may also present with weight loss. Anemia results in signs of weakness, pallor of the mucous membranes, tachypnea, tachycardia, and occasionally syncope. Some owners may report their cat eats dirt, litter, or licks cement. Other physical examination abnormalities may include cardiac murmurs, sometimes splenomegaly, and icterus. Some cats may be febrile, and moribund cats may be hypothermic.

Answer 110

Autoagglutination may be noted in blood smears from some infected cats. The most characteristic abnormality on the CBC is regenerative anemia, with anisocytosis, reticulocytosis, polychromasia, Howell-Jolly bodies, and sometimes marked normoblastemia. Nonregenerative anemia may also be noted. In some cases this is because sufficient time for a regenerative response has not yet elapsed. In others, anemia is nonregenerative as a result of concurrent FeLV infection, although macrocytic, normocytic nonregenerative anemias have been documented in FeLV-negative cats with hemoplasmosis. White blood cell counts may be normal, elevated, or low.

Answer 111

Concurrent occult infection with hemoplasmas (even in the absence of reticulocytosis).

Answer 112

Primary immune-mediated hemolytic anemia, Other infectious causes of anemia such as cytauxzoonosis, Feline infectious peritonitis virus Feline retrovirus infections Heinz body hemolytic anemia, Inherited erythrocyte disorders such as pyruvate kinase deficiency Red cell fragility disorder of Abyssinian and Somali cats.

Answer 113

Treatment is indicated for cats and dogs with clinical signs and laboratory abnormalities consistent with hemoplasmosis. Treatment of PCR-positive, healthy animals is currently not recommended, as no regimen has yet been identified that completely eliminates the organism. The treatment of choice for hemoplasmosis is doxycycline.

Answer 114

Nosocomial Infection and Resistant Bacteria: The term nosocomial is used to describe infections that are not present on admission but that develop more than 48 hours into hospitalization, or to infections occurring in a patient that has been hospitalized in the 2 weeks prior to the current admission. (Health care–associated infections (HAI)) HAI may be caused by many pathogens; however, a substantial proportion are caused by multidrug resistant organisms. For example, in people the proportion of hospital-acquired staphylococcal infections caused by methicillin-resistant (as opposed to methicillin-sensitive) Staphylococcus aureus is greater than 35% in the United Kingdom and up to 64% in the United States

Answer 115

Staphylococci: Staphylococci are gram-positive cocci that are a common commensal of mucosa and skin but can cause a wide range of infections. Methicillin-resistant S. aureus (MRSA) is one of the most significant bacteria causing HAI in human medicine and has been identified with increasing frequency in veterinary patients. MRSA has acquired the mecA gene, resulting in production of an altered penicillin-binding protein and resistance to all beta-lactam antimicrobials.

Answer 116

Antimicrobial treatment should be based on culture and sensitivity testing. Many MRSA isolates are sensitive to commonly used antimicrobial agents such as trimethoprim-sulpha and tetracyclines, and these antimicrobials are recommended for the treatment of non–life-threatening infections. Vancomycin is the intravenous antibiotic of choice for human patients with MRSA sepsis but experience in the veterinary setting is limited. Methicillin-resistant S. pseudintermedius (previously known as S. intermedius) has been reported recently as causing disease in canine and feline patients; the emergence of resistant S. pseudintermedius is potentially a greater concern to veterinary patients as it is the principle staphylococcal species colonizing healthy dogs. Coagulase-negative Staphylococci may also be implicated in nosocomial infection and may be found contaminating the veterinary environment.

Answer 117

Enterococci are gram-positive facultative cocci that are commonly found colonizing the mammalian gastrointestinal tract. Previously categorized as streptococci, the genus Enterococcus was only recognized as a distinct taxonomy in 1984. E. faecium and E. faecalis are the most common enterococci causing HAI in people. They are generally considered to be of relatively low virulence but are capable of causing a wide range of infections including sepsis. Enterococci are inherently resistant to many antimicrobials and are efficient at acquiring new resistance mechanisms. The acquisition of the vanA or vanB gene complexes led to the emergence of vancomycin-resistant E. faecium (VRE) in human patients.

Answer 118

The Enterobacteriaceae group includes Escherichia coli, Klebsiella spp., and Enterobacter spp. These gram-negative bacteria are commensals of the gastrointestinal tract and are emerging as a significant public health concern in human medicine. Production of beta-lactamases by these bacteria has been documented since before beta-lactam antibiotics were used in clinical practice; however, the spectrum of beta-lactam antimicrobials against which the beta-lactamases are effective is expanding. Of particular concern are the Enterobacteriaceae, which produce extended-spectrum beta-lactamases (ESBLs) and extended-spectrum cephalosporinases (ESCs). The classification system used for beta-lactamases is complex, but essentially certain beta-lactamase enzymes (e.g., TEM and SHV) have evolved such that they can hydrolyze not only the small penicillin molecules but also the larger cephalosporins. Other newly identified beta-lactamase enzymes such as CTX-M are also being found in E. coli and Klebsiella. Reports of ESBL Enterobacteriaceae causing clinical disease in veterinary patients are limited.

Answer 119

Pseudomonas aeruginosa is a gram-negative bacterium that is ubiquitous in the environment. Its ability to survive especially in moist environments contributes to its success as an opportunistic nosocomial pathogen. It possesses a high level of intrinsic resistance due to a number of mechanisms including a highly impermeable outer membrane, broad spectrum multidrug efflux system, and its ability to produce biofilms.

Answer 120

Acinetobacter spp. are gram-negative aerobic coccobacilli. A. baumanii is the commonest Acinetobacter species implicated in HAI in both human and veterinary patients.

Answer 121

Other bacteria that have been associated with outbreaks of nosocomial infections in small animal patients include multidrug-resistant Salmonella typhimurium in four animal facilities in the United States and Clostridium difficile. C. difficile may be found in the feces of hospitalized dogs and cats and in the veterinary environment. It has been responsible for outbreaks of enteric disease.

Answer 122

Feline immunodeficiency virus (FIV) is a lymphotropic lentivirus that, like HIV in humans, causes an acquired immunodeficiency syndrome (AIDS) in domestic cats. FIV is related morphologically and biochemically to HIV but is antigenically distinct. Both viruses also share a similar pattern of pathogenesis, characterized by a long period of clinical latency during which immune function gradually deteriorates. Eventually, AIDS develops, accompanied by opportunistic infections, systemic diseases, and malignancies. It is the close relationship between HIV and FIV that has kindled interest in the use of FIV as an animal model for the study of lentiviral immunopathogenesis. Field strains of FIV are divided into 5 subgroups, or clades (A-E), based on sequence differences in the envelope gene. Cats in the United States are most commonly infected with A, B, and occasionally C strains. Some cats harbor multiple strains or strain recombinants.

Answer 123

Most cases of FIV infection are acquired by horizontal transmission among adult cats. Worldwide, adult male cats living outdoors consistently compose the majority of FIV-infected cats, and the risk is highest for sexually intact males. Infectious virus is found in the saliva of FIV-positive cats, and the fighting and biting behavior of this group of cats is believed to be the main source of transmission. Interestingly, sexual transmission, the most common mode of transmission of HIV, appears to be unusual in FIV, even though the semen of infected cats frequently contains infectious virus.

Answer 124

Identification and segregation of infected cats is considered to be the single most effective method for preventing new infections with FIV.

Answer 125

Mild clinical signs associated with acute FIV infection, including transient fever, lymphadenopathy, and leukopenia, are likely to pass unnoticed by cat owners. High concentrations of virus in the blood can be detected by culture and PCR within 2 weeks of infection. Simultaneously, both CD4+ (helper) and CD8+ (cytotoxic-suppressor) T lymphocytes decline, followed by a vigorous immune response. This response includes a recovery of CD8+ T lymphocytes to greater than preinfection levels, the production of FIV antibodies, and a decrease of circulating viral load.

Answer 126

Both CD4+ and CD8+ T lymphocytes gradually decline, and an inversion of the CD4+:CD8+ T lymphocyte ratio persists for the rest of the cat's life. Infected lymphocytes and macrophages carry the virus to other organs, but lymphoid tissues remain the primary site of viral replication. Other immune disruptions include changes in cytokines (increased expression of proinflammatory cytokines interleukin [IL]-4, IL-6, IL-10, interferon gamma, and tumor necrosis factor; decreased expression of IL-2 and IL-12), and decreased natural killer cell activity, mitogen responsiveness, memory cell activity, and neutrophil function. These changes lead to a decrease in cell-mediated immunity. Simultaneously, increased B cell activity and nonspecific immunoglobulin production are associated with polyclonal gammopathy.

Answer 127

Some cats with severe CD4+ T lymphocytopenia remain healthy for many years. Following acute infection, FIV-infected cats enter a prolonged asymptomatic stage during which progressive dysfunction of the immune system occurs. Chronic inflammatory conditions, neoplasia, and infections with intracellular organisms are more common than infections controlled by antibodies in FIV-infected cats. FIV-infected cats also appear to respond adequately to vaccination. These findings reflect the fact that cell-mediated immunity is more profoundly affected than humoral immunity.

Answer 128

Weight loss Fever Oral infections/stomatits Dehydration Rhinitis conjunctivitis, ocular inflammation (uveitis and chorioretinitis) abscesses Renal disease Anemia and leukopenia Upper respiratory infections Neoplasia (especially lymphoma and cutaneous squamous cell carcinoma)

Answer 129

Chronic ulceroproliferative stomatitis is the most common disease syndrome induced in cats with longstanding FIV infection. Interestingly, this syndrome occurs mainly in cats that are also exposed to other infectious agents in addition to FIV and does not readily develop in FIV-infected SPF cats. Concurrent calicivirus infection is often identified in the oral cavity of cats with FIV-associated stomatitis and may be one of the infectious cofactors capable of inducing stomatitis in combination with FIV. Histologically, the mucosa is invaded by plasma cells and lymphocytes, accompanied by variable degrees of neutrophilic and eosinophilic inflammation. The cause of the syndrome is uncertain, although the histologic findings suggest an immune response to chronic antigenic stimulation or immune dysregulation.

Answer 130

AZT is the most thoroughly studied anti-FIV drug in cats. AZT reduces plasma virus load and improves CD4+ cell count, but it is not known if treatment results in prolonged health or survival (“Routine vaccination” of retrovirus-infected cats is a subject of debate. Vaccination of FIV-infected cats may lead to stimulation of the immune system and subsequent increased FIV replication, although the clinical significance of this observation is unknown.)

Answer 131

it appeares to be spread both vertically (from queen to kitten) and horizontally (from cat to cat). The infection is associated with a variety of illnesses in addition to neoplasia, including bone marrow suppression and immunodeficiency

Answer 132

FeLV is a retrovirus. Its genetic material is transmitted as RNA, which is reverse transcribed into DNA within infected cells. The DNA copies are inserted randomly into the host genome. Once this DNA provirus is integrated, cell divisions will result in daughter cells that also contain the viral DNA.

Answer 133

The virus encodes several major protein groups: gag (group-specific antigens), pol (reverse transcriptase), and env (envelope). One of the gag proteins, p27, is abundant in the plasma of infected cats and in the cytoplasm of individual infected cells. This protein is the basis for most currently used diagnostic tests. The envelope protein gp70 defines the virus subgroup and appears to be important for inducing immunity.

Answer 134

Male gender, adulthood, illness, outdoor access, Certain diseases are associated with a high prevalence of FeLV infection, such as cutaneous abscesses and bite wounds, and oral inflammation Whereas indoor lifestyle and sterilization are associated with reduced infection rates.

Answer 135

Horizontal transmission of FeLV among susceptible cats occurs most commonly via the oronasal route and by bite wounds. After mucosal or cutaneous inoculation of FeLV, the virus replicates in local lymphoid tissues. From there, infected cells carry the virus to other target tissues, such as thymus, spleen, and lymph nodes. At this stage of acute viral replication, fever, malaise, diarrhea, and leukopenia are common. In addition, generalized lymphadenopathy may be so marked as to be mistaken for lymphoma.

Answer 136

Regardless of the eventual outcome of infection, all cats appear to develop similar proviral and plasma viral RNA loads during early infection.[9] The virus later populates salivary glands and mucosal glandular epithelium. These sites of infection may secrete most of the infectious virus that is responsible for horizontal transmission. About the same time, bone marrow cells become involved, producing infected leukocytes and platelets that circulate in the blood.

Answer 137

Although somewhat controversial, FeLV infection is currently described as having two common outcomes (progressive or regressive infection) and two uncommon outcomes (abortive exposure or focal infection).

Answer 138

In progressive infection, insufficient FeLV-specific immunity results in extensive virus replication that occurs first in the lymphoid tissues and then in the bone marrow. Spread to mucosal and glandular tissues and excretion of infectious virus occurs simultaneously with bone marrow infection. Most cats are persistently antigenemic and frequently succumb to FeLV-associated diseases within a few years.

Answer 139

In regressive infection, an effective immune response limits virus replication prior to or at the time of bone marrow infection. FeLV antigen is usually detectable in peripheral blood within 2 to 3 weeks after virus exposure but then disappears 2 to 8 weeks later or, in rare cases, even after many months. Rarely, some infected cats fail to ever develop detectable antigenemia. The clinical relevance of regressive infections is not yet clear. Cats with regressive infection have persistent integration of FeLV DNA in their genome, but are unlikely to develop FeLV-associated diseases. Even though viral shedding does not occur, it is possible that cats with regressive infection can still transmit FeLV via blood and tissue donation since the proviral DNA might be infectious

Answer 140

Two other outcomes of FeLV exposure occur less commonly and are more poorly understood. Abortive exposure has been observed infrequently following experimental FeLV inoculation and is characterized by negative test results for culturable virus, antigen, viral RNA, and proviral DNA after FeLV exposure. Focal infections are described as rare events in which cats have FeLV infection restricted to certain tissues, such as the spleen, lymph nodes, small intestine, or mammary glands.

Answer 141

including anemia, lymphoma, and susceptibility to secondary and opportunistic infections

Answer 142

Free of clinical signs. Weight loss Fever Dehydration Rhinitis Diarrhea Conjunctivitis Oral inflammation Lymphadenopathy Abscesses

Answer 143

Bone marrow suppression is the most common clinical syndrome associated with FeLV infection and results from viral infection of both hematopoietic stem cells and bone marrow stromal cells that constitute the supporting environment for hematopoietic cells.

Answer 144

The most common form of FeLV-induced anemia is pure red cell aplasia, a severe nonregenerative anemia associated with marked depletion and maturation arrest of erythroid precursors in the bone marrow. Serum erythropoietin concentrations are markedly increased, and few cats with FeLV-associated anemia respond to exogenous erythropoietin therapy.

Answer 145

Regenerative anemia in FeLV-infected cats, indicated by increased reticulocytes and, in some cases, nucleated RBCs, is less common than nonregenerative anemia and is often associated with coinfection with Mycoplasma haemofelis and Mycoplasma haemominutum.

Answer 146

Approximately one third of cats with immune-mediated hemolytic anemia are FeLV-positive; in some cases, hemolysis precedes the emergence of myeloproliferative disease or lymphoma.

Answer 147

Diagnostic evaluation of anemic FeLV-infected cats should include a complete blood count (CBC), reticulocyte count, serum chemistry panel, Coombs' test, and bone marrow evaluation when indicated.

Answer 148

PCR is the best method for diagnosis of M. haemofelis or M. haemominutum infection. If a specific cause for anemia is not determined, treatment should include a course of doxycycline to rule out occult hemoplasmosis. Prednisone at antiinflammatory or immunosuppressive doses may improve nonregenerative anemia in some cats.

Answer 149

FeLV is the most common cause of thrombocytopenia and granulocytopenia in cats. FeLV and myeloproliferative diseases accounted for 44% of cats with thrombocytopenia in one report. Cyclic and persistent neutropenia have been observed. An immune-mediated mechanism may be involved, since some cats respond to treatment with prednisone.

Answer 150

Various cytopenias may wax and wane in FeLV-infected cats, seemingly responding to a variety of therapeutic interventions. Some persistent cytopenias are associated with myelodysplasia and may eventually evolve into a terminal myelodysplastic syndrome or leukemia. In addition to the direct bone marrow suppressive effects of FeLV, nonregenerative anemia, leukopenia, and thrombocytopenia may also be a consequence of secondary effects of the virus, including bone marrow infiltration with lymphoma, leukemia, infectious agents, myelofibrosis, and osteosclerosis.

Answer 151

The most common tumors associated with FeLV infection are those of the lymphoid and hematopoeitic systems. FeLV-infected cats have sixtyfold increased risk of developing lymphoma compared with FeLV-negative cats. Lymphoma may affect up to one in four cats infected with FeLV, usually within 2 years after diagnosis of the viral infection.

Answer 152

Multicentric and mediastinal lymphoma are the most common forms to occur in FeLV-positive cats. Although less common, spinal, renal, ocular and other forms of lymphoma are also reported in young FeLV-infected cats. As the prevalence of FeLV decreased since its discovery, so has the incidence of lymphoma. When FeLV was more prevalent, mediastinal and multicentric were the most common forms of lymphoma diagnosed in cats. Now that FeLV is less prevalent, alimentary lymphoma is the most common form diagnosed and a majority of affected cats are middle-aged or geriatric and free of FeLV antigen.[5] However, FeLV may still play a role in lymphoma development in some cats that test negative

Answer 153

Myelodysplasia (preleukemia) is characterized by nonregenerative anemia accompanied by abnormalities in cellular maturation in the bone marrow. Granulocytopenia and thrombocytopenia may also occur. Most cats are positive for FeLV. Bone marrow is usually hypercellular, and many samples also exhibit myelofibrosis. Blast cells comprise less than 30% of the marrow elements, distinguishing myelodysplasia from leukemia. Progression to acute leukemia is common and may occur within weeks to months after the diagnosis of myelodysplasia.

Answer 154

Treatment with immunosuppressive doses of corticosteroids and blood transfusions may palliate clinical signs, but the prognosis is poor for most cats that have myelodysplasia-associated bone marrow suppression.

Answer 155

Nearly all cats with acute nonlymphoid leukemia (ANLL or acute myeloid leukemia) are FeLV-positive. This disease can involve erythroid elements (erythemic myelosis, erythroleukemia, reticuloendotheliosis), myeloid elements (granulocytic, monocytic, or myelomonocytic leukemia), or megakaryocytes. Stem cell involvement may result in a sequential expression of leukemia of various cell lines.

Answer 156

Prognosis is grave for ANLL because chemotherapy does not appear to alter the course. Most cats are euthanized within days to weeks of diagnosis. Heavy infiltration of bone marrow (and frequently other organs) with lymphoblasts characterizes acute lymphocytic leukemia (ALL). ALL is often accompanied by anemia and circulating blasts. Most cats with ALL are FeLV-positive. Differentiating ALL from advanced lymphoma can be difficult, although the treatment for both forms of lymphoproliferative disease is similar.

Answer 157

Chronic lymphocytic leukemia (CLL) is uncommon, tends to occur in older FeLV-negative cats, and carries a better prognosis than ALL. Hypereosinophilic syndrome, polycythemia vera, and multiple myeloma are proliferative hematologic disorders that are not associated with FeLV infection.

Answer 158

Diseases associated with immune suppression account for much of the morbidity and mortality in FeLV-infected cats. Thymic atrophy and depletion of lymph node paracortical zones are common findings, particularly in cats infected as kittens. Neutropenia and lymphopenia may further exacerbate immune suppression. Several immune function tests reportedly are abnormal in FeLV-infected cats, including poor response to T cell mitogens, prolonged allograft rejection, reduced immunoglobulin production, depressed neutrophil function, complement depletion, cytokine dysregulation, and poor responses to vaccination.

Answer 159

Many case reports exist of FeLV-infected cats having concurrent bacterial, viral, protozoal, and fungal infections; however, few studies prove these cats have a higher rate of infection than FeLV-negative cats or that they have a less favorable response to therapy. Thus, although FeLV is well known to suppress immune function, it should not be assumed that all concurrent infections are a result of FeLV infection. The most common secondary infections associated with FeLV are respiratory viruses that persist longer and cause greater illness than observed in immune competent cats. Hemoplasmosis, which may be clinically silent in healthy cats, is more likely to be associated with severe hemolytic anemia in FeLV-coinfected cats. FeLV-infected cats residing in households endemic for coronavirus are more likely to develop fatal FIP than are housemates free of FeLV. Treatment-resistant dermatophytosis and acute generalized toxoplasmosis are associated with FeLV infection.

Answer 160

Reproductive failures have been associated with abortion due to endometritis or transplacental infection of fetuses. Glomerulonephritis Transient generalized lymphadenopathy has been observed in young cats and may be mistaken for lymphoma. A “panleukopenia-like syndrome” of FeLV mimics feline parvovirus infection and is characterized by panleukopenia, crypt necrosis, and high mortality. In some cats, parvovirus is identified as a coinfection. Neurologic infection has been reported to cause urinary incontinence and papillary spasm leading to D-shaped pupils and anisocoria. FeLV-associated myelopathy results in vocalization, hyperesthesia, and paresis progressing to paralysis. Lymphocytic-plasmacytic stomatitis, although more common in cats infected with FIV, is also increased in FeLV-infected cats

Answer 161

Protection is not absolute, so vaccination against FeLV should not be used as a substitute for testing to identify and isolate infected cats. Cats should be tested for infection before initial FeLV vaccination because administration of FeLV vaccines to cats already infected with FeLV is not believed to have any value.

Answer 162

Adherence to guidelines to test all cats for FeLV is likely to result in the identification of many asymptomatic cats. Early identification permits actions to prevent the spread of infection through segregation and to optimize the health of infected cats. PCR testing may create a new dilemma regarding the appropriate management of cats with regressive infection because FeLV provirus is infectious

Answer 163

Feline infectious peritonitis (FIP) is an immune-mediated disease, triggered by infection with a feline coronavirus (FCoV) that belongs to the family Coronaviridae, enveloped, positive-stranded RNA viruses. FCoV is transmitted by the fecal-oral route between felids but is not infectious for other species (including humans). Coronavirus-specific antibodies are present in up to 90% of cattery cats and in up to 50% of those in single-cat households; however, only about 5% of FCoV-infected cats develop FIP in a multicat household

Answer 164

It had been hypothesized that there are two different virus species in cats, FCoV that cause FIP (FIPV) and “harmless” enteric FCoV (FECV). It is now known, however, that there is only one FCoV, and that FCoV strains with different behavior simply represent virulence variants of the same virus.

Answer 165

Cats are primarily infected with avirulent FCoV strains that replicate in enterocytes. In some instances, however, a mutation occurs in a certain region of the FCoV genome[9],[10] that codes for a new phenotype with the ability to replicate within macrophages; this is a key pathogenic event in the development of FIP. If the cat fails to eliminate the cells infected with the mutated virus soon after the mutation has taken place, the presence of the virus within macrophages Serum initiates the ultimately fatal immune-mediated reaction that defines FIP.

Answer 166

Affected cats develop signs caused by granulomatous lesions in the target organs (central nervous system, eyes, and parenchymatous organs) and vasculitis leading to fluid redistribution into third spaces with fluid accumulation in body cavities, including pericardium. In addition to the well-known condition, some unusual problems have been described. Skin fragility syndrome was recognized in a cat with FIP,[11] and other skin lesions (e.g., skin papules and nodules, pododermatitis) have been reported. Intestinal manifestations and masses in the abdominal cavity have been described.

Answer 167

Blood cell counts are often altered in cats with FIP, but the changes are not pathognomonic. White blood cell counts can be both decreased or increased. Lymphopenia is commonly present and is mainly caused by apoptosis of uninfected T cells, primarily CD8+ T cells, as a result of high tumor necrosis factor-α (TNF-α) concentrations produced by virus-infected macrophages.[19] However, lymphopenia in combination with neutrophilia is generally common in cats as a typical “stress leukogram” that can occur in many severe diseases.

Answer 168

The most consistent laboratory finding in cats with FIP is an increase in total serum protein concentration caused by a rise in globulins, mainly γ-globulins. Antibody titers and hypergammaglobulinemia show a linear correlation, but the wide variation in anti-FCoV titers at a given concentration of γ-globulins indicates that additional (autoimmune) reactions occur. It is possible that stimulation of B cells by interleukin-6, produced as part of the disease process, also contributes to the increase in γ-globulins.

Answer 169

total protein levels in cats with FIP can reach concentrations of 120 g/L (12 g/dL) and higher. The albumin to globulin ratio has a significantly higher diagnostic value than either total serum protein or γ-globulin concentrations, because a decrease in serum albumin also commonly occurs through a decrease in production in association with liver failure or protein loss.

Answer 170

1. glomerulopathy secondary to immune complex deposition 2. by loss of protein due to exudative enteropathy in case of granulomatous changes in the intestines 3. by extravasation of protein-rich fluid during vasculitis.

Answer 171

An optimal cutoff value (maximum efficiency) of 0.8 was determined for the albumin-to-globulin ratio. Serum protein electrophoresis has been recommended mainly to distinguish a polyclonal from a monoclonal hypergammaglobulinemia. This is done in order to differentiate FIP from tumors such as plasmocytomas. However, in cats with FIP, both polyclonal and monoclonal hypergammaglobulinemia can occur, same as is seen in tumors. Therefore, the value of electrophoresis is limited.

Answer 172

Other laboratory parameters (liver enzymes, bilirubin, BUN, creatinine) can be variably elevated depending on the degree and localization of organ damage, but are not helpful in establishing an etiological diagnosis. Hyperbilirubinemia and icterus are often observed and frequently are a reflection of hepatic necrosis, despite the fact that ALP and ALT activities are often not increased as dramatically as they are with other liver diseases, such as cholangiohepatitis and hepatic lipidosis. Sometimes, bilirubin is increased without evidence of hemolysis, liver disease, or cholestasis; this unusual change is otherwise only observed in septic animals. Bilirubin metabolism and excretion into the biliary system is compromised in these cats due to high levels of TNF-α that inhibit transmembrane transport.

Answer 173

Immune-suppressive drugs such as prednisone or cyclophosphamide may slow disease progression. Some cats with effusion benefit from “tapping” and removal of the fluid and injection of dexamethasone into the abdominal or thoracic cavity. Cats should also be treated with broad-spectrum antibiotics and supportive therapy (e.g., fluids) in addition to the immune-suppressive treatment. (Some veterinarians prescribe immune modulators (e.g., promodulin, acemannan) to treat cats with FIP with no documented controlled evidence of efficacy). The search for an effective antiviral compound has not been successful. Preventing FIP is extremely difficult. The only way to truly prevent the development of FIP is to prevent infection with FCoV.

Answer 174

FELINE VIRAL RESPIRATORY DISEASE Feline viral respiratory disease is most commonly seen where cats are grouped together, such as in breeding and boarding catteries, and in rescue shelters. The two main causes of viral respiratory disease in cats are feline herpesvirus (FHV-1) (feline rhinotracheitis virus) and feline calicivirus (FCV). FHV-1 generally induces a more severe disease than FCV, but FCV appears to be relatively more common. Other viruses implicated in the syndrome include feline reovirus and cowpox virus (see following). Bacterial pathogens such as Bordetella bronchiseptica and Chlamydophila felis may also be involved in infectious respiratory disease in cats.

Answer 175

FHV-1 is an alphaherpesvirus affecting both domestic cats and other members of the Felidae. Only one serotype of the virus exists, and genetically all isolates are similar. The virus contains double-stranded DNA and is enveloped, making it relatively labile.

Answer 176

FCV is a small nonenveloped RNA virus. Only one genotype and one serotype of the virus exist, although a large degree of variability exists within both of these. Most strains of FCV are closely related enough antigenically to induce some degree of cross-protection and this has been utilized in developing vaccines. FCV affects both domestic cats, and some nondomestic Felidae. Although dogs have their own genetically distinct calicivirus, some canine calicivirus isolates appear to be closely related to FCV.[7] FCV can persist in the environment for up to several weeks, compared to a day or so for FHV-1, and is less susceptible to some disinfectants.

Answer 177

FHV-1 causes upper respiratory tract (URT) disease, with oculonasal discharges, conjunctivitis, sneezing, and sometimes hypersalivation and coughing. Occasionally more severe signs including pneumonia and generalized disease may be seen, particularly in young or debilitated animals. Abortion occurs rarely, and is probably due to severe systemic disease and not due to the virus itself. The role of FHV-1 in conjunctivitis and, in some cases, ulcerative keratitis, has long been known. However, improved viral detection using PCR has led to increasing recognition of this role in the acute disease as well as in more chronic ocular lesions such as stromal keratitis. Similarly, involvement of FeHV-1 with skin ulcers and dermatitis has also been described

Answer 178

In FCV infection, because of the large number of different strains, there is some variation in clinical signs. The most characteristic sign is oral ulceration, typically on the tongue, but lesions may sometimes occur elsewhere in the mouth or on the skin. Classic URT disease signs, such as ocular and nasal discharges and conjunctivitis, also commonly occur, but these are generally milder than those seen with FHV-1. With some strains of FCV, lameness and pyrexia may be a feature, with or without respiratory/oral disease; other strains may induce an interstitial pneumonia, and some appear apathogenic. In addition, FCV infection is associated with chronic stomatitis, although its precise role in the condition is not clear and other factors are likely to be involved.

Answer 179

In addition to URT disease, affected cats show to varying degrees pyrexia, cutaneous edema, ulcerative dermatitis, anorexia, and jaundice, with a high mortality rate. Adult cats are frequently affected more severely than kittens, and field vaccination does not appear to be protective. Each outbreak appears to be caused by a different strain; so far none of these VS-FCVs appear to have become widely established in the population.

Answer 180

Treatment involves both broad-spectrum antibacterial cover, and supportive therapy. Tetracyclines are indicated if Bordetella bronchiseptica or Chlamydophila felis are involved. No specific antivirals are widely used for either FHV-1 or FCV infection.

Answer 181

Both viruses are primarily transmitted by direct contact between cats, although indirect transmission may also occur in the short term through contact with infectious discharges. Aerosols are not of major importance, although sneezed macrodroplets may transmit infection over a distance of 1 to 2 meters. Acutely infected cats are clearly an important source of virus, but infection also commonly occurs from clinically recovered carrier cats. In FHV-1 carriers, the virus persists in a latent form largely in trigeminal ganglia, though other tissues may also be involved. Periodically, particularly after a stress, virus reactivates in such carriers and they can then infect other animals. Stresses that may induce virus shedding include a change of housing, kittening and lactation, and corticosteroid treatment. Some cats may show clinical signs during a reactivation episode, which can be a useful indicator that they are likely to be infectious. Unlike FHV-1 carriers, FCV carriers shed virus more or less continuously and are therefore always infectious to other cats. The virus persists in tonsil and other oropharyngeal tissues. In some cats the carrier state appears to be lifelong, but most stop shedding and appear to eliminate virus at some point. FCV carriers appear to be common, with approximately 20% to 30% of cats in the general population shedding FCV and up to 90% in rescue shelters and colonies. From recent studies of endemically infected colonies, it appears that only a minority of such cats are true persistent shedders; the majority are undergoing cycles of reinfection from other cats in the environment.

Answer 182

Influenza viruses are known to be able infect cats, although until recently it was thought this was not associated with disease. Following the identification of humans infected with highly pathogenic bird flu strain H5N1, it has been recognized that this virus can naturally infect and cause disease in cats, and this can be reproduced experimentally.

Answer 183

Feline panleukopenia is caused by a parvovirus, a small, nonenveloped DNA virus similar to the canine parvovirus type 2 (CPV-2), which causes a severe hemorrhagic enteritis in dogs. CPV-2 has largely been replaced by CPV-2a and CPV-2b, which now coexist in dog populations worldwide. Although CPV-2 isolates did not replicate in cats, both CPV-2a and CPV-2b do so and have been reported to constitute a small proportion of isolates found naturally in cats.

Answer 184

The rapidly dividing cells of : 1. Lymphoid tissue 2. The bone marrow, leading to panleukopenia, and the crypt epithelium of the intestinal mucosa, leading to enteritis.

Answer 185

Fetal death and resorption. From the middle third of gestation to immediately postnatally, infection may result in cerebellar hypoplasia in kittens.

Answer 186

Lethargy, fever, and anorexia with apparent thirst but refusal to drink. Affected cats may vomit, particularly in the early stages. Profuse watery diarrhoea or dysentery then develops and cats may become severely dehydrated. Most fatalities occur within 3 to 5 days of the first signs of illness and are probably due to overwhelming bacterial infection, dehydration, and electrolyte imbalance. Experimental infections have suggested that infection with CPV in cats may lead to milder disease with reduced virus shedding compared to FPV, although the situation in the field is unclear.

Answer 187

Ataxia, incoordination, hypermetria, and often intention tremors. These signs persist for life. Nevertheless, affected kittens may learn to compensate and otherwise function normally. Other findings: Forebrain lesions have been reported and may lead to seizures and behavioral abnormalities. Retinal lesions may also be present but are usually of no clinical significance. A possible role of FPV in myocarditis and idiopathic cardiomyopathy has also been suggested. . Diagnosis may also be confirmed at necropsy, where characteristic histopathologic changes, including the presence of intranuclear inclusion bodies, may be seen in the crypt epithelium of the small intestine

Answer 188

RNA virus Affected cats show motor dysfunction and behavioral changes including an unsteady “staggering” gait, depression, and progressive hindlimb ataxia and paresis. Other signs include anorexia, increased salivation, hyperesthesia, impaired vision, and seizures. The disease is generally progressive, and despite supportive treatment, affected cats die or are euthanized. At necropsy there is a characteristic nonsuppurative meningoencephalomyelitis mainly in the grey matter of the cortex, brainstem, and spinal cord.

Answer 189

Cats are susceptible to cowpox virus, a member of the Orthopoxvirus family. Occasional cases of parapoxvirus infection in cats have also been reported. Feline foamy virus (FFV) is a member of the foamy virus group (spumaviruses) in the retrovirus family. Spumaviruses have been isolated from many species, but they generally do not appear to be pathogenic.

Answer 190

Clinical disease appears to be uncommon and diarrhea, when it occurs, tends to be mild and of only short duration

Answer 191

The term rabies describes an acute fatal disease of the nervous system caused by viruses in the genus Lyssavirus, family Rhabdoviridae. The viruses are bullet-shaped and enveloped with a negative-sense, single-stranded genome. The species of animals in which these viruses are perpetuated are restricted to the orders Chiroptera (bats) and Carnivora. Mammals are susceptible to rabies in varying degrees; the disease does not occur in amphibians, reptiles, birds, or invertebrates.

Answer 192

The predominant and natural route for rabies virus transmission is via bite wounds. Within the reservoir host of a particular rabies virus variant, viral infection results in exquisite behavioral changes that may favor transmission via contact. For example, viral infection may result in abnormal vocalization by an adult animal that mimics the call of a juvenile animal. Other animals, and particularly those of the same species, may be more likely to investigate the source of this vocalization, which would enhance opportunities for bite encounters and transmission to the next host. Contact transfer of rabies by either animate or inanimate objects has not been found to result in naturally occurring cases. Thus, beyond a direct bite from a rabid animal, contamination of an open bleeding wound with infectious material such as saliva, or tissue from a rabid animal that contains nervous system components, is clearly an exposure to rabies. The natural history of rabies virus transmission does not rely upon aerosolization although it is clear that artificially created aerosols present a potent risk of infection. Rabies viruses are relatively fragile. Once saliva or contaminated tissue has dried, the material is no longer infectious.

Answer 193

Nonspecific: General lethargy, inappetence, diarrhea vomiting.

Answer 194

Changes in behavior Rabies is neurotropic and may result in irritation or paresthesia at the site of initial exposure even though the inflicted wound may have healed. A combination of increased saliva production and a decreased ability to swallow may present as profound contamination of the mouth, chin, and forelegs with potentially infectious saliva. Cranial nerve involvement may be focal and unilateral, presenting as unequal pupil size with dysfunction, facial or tongue paresis, and changes in phonation. As the clinical period progresses, unpredictable episodes of attempts to bite may be invoked by auditory, visual, or tactile stimuli with aggression to the point of self-mutilation. In the end stage, most animals become profoundly moribund.

Answer 195

6 months following exposure.

Answer 196

Virus is introduced into local tissues through a bite from the infectious host. There may be viral replication locally but only in limited amounts. The virus is highly neurotropic; there is no viremia or shedding in the urogenitary or gastrointestinal tract. Still unpredictable is the timing of when viral infection progresses from local neurons at the site of infection to the central nervous system. The incubation period is variable and is generally inversely related to viral dose and severity of exposure. The majority of infected animals become clinically rabid in several weeks to several months following exposure. On the basis of experimental and field data, a 6-month quarantine (or euthanasia to prevent the development of rabies) is imposed on exposed, unvaccinated (or outdated) domestic animals, as this is considered a probable maximum incubation period.

Answer 197

Once virus reaches the central nervous system, infection may spread quickly through numerous neuronal tracts. Thus, the clinical period is relatively brief; on the order of days rather than weeks. Once the brain is infected, virus is then capable of spreading centrifugally from the central nervous system through innervations to major organ systems as long as the host remains alive. Virus is produced in high amounts in the salivary glands leading to the presence of virus in the saliva. Profound neuronal dysfunction occurs and, even with assisted preservation of an airway and ventilation, may manifest as autonomic instability sufficient to result in death.

Answer 198

10-day period. If there were a risk of viral shedding and transmission, the animal would have manifested signs of clinical rabies (sometimes including acute death) during the observation period. If an animal develops clinical illness compatible with rabies (or dies acutely or is euthanized due to lack of ownership or concerns about viciousness) during the 10-day period, it should be humanely euthanized. After euthanasia, the body should be tested for rabies as soon as possible.

Answer 199

Oronasal exposure to virus-contaminated vomitus, feces, and environmental fomites. The virus can also be spread by rodents, birds, and insects.

Answer 200

The incubation period ranges from 3 to 14 days but is typically 5 to 7 days. Virus shedding in feces begins 3 to 4 days after exposure during the preclinical incubation period and continues intermittently for up to 2 weeks. Dogs with subclinical infection also shed virus in feces. Thus, infected dogs may be contagious for up to 30 days after exposure.

Answer 201

Lymphoid cells in the oropharynx, mesenteric lymph nodes, and thymus.

Answer 202

The gastrointestinal (GI) tract, lymphoid tissues, bone marrow. Virus replication occurs in epithelial cells lining the oral cavity, tongue, esophagus, small intestinal crypts, lungs, liver, kidneys, lymphoid organs, bone marrow, and (in young animals) myocardial cells.

Answer 203

Necrosis of infected intestinal crypt cells leads to villus collapse and loss of intestinal epithelial integrity. The hemorrhagic diarrhea characteristic of the clinical disease results from a combination of increased intestinal permeability and malassimilation from abnormal mucosal function. Breakdown of the intestinal epithelial barrier predisposes to translocation of intestinal bacteria and absorption of bacterial endotoxins into the systemic circulation (common events in parvoviral-infected dogs).

Answer 204

Sepsis, endotoxemia, the systemic inflammatory response syndrome (SIRS), disseminated intravascular coagulation (DIC), and death. SIRS has been associated with higher mortality rates. Activation of systemic immune responses also increases the risk of thromboembolic complications. Lymphopenia and, in some cases, pancytopenia result from viral destruction of myeloproliferative cells in the bone marrow.

Answer 205

Often start with anorexia, lethargy, and fever. The condition progresses within 1 to 2 days to include vomiting and diarrhea, which may be yellow, mucoid, or hemorrhagic. More severe GI signs can be expected in puppies with intestinal parasites or other concurrent intenal disease. Uncommonly, clinical signs of myocarditis may be observed in puppies, typically those younger than 8 weeks of age with failure of passive transfer of maternal immunity. These puppies may die acutely or after exhibiting signs of enteric disease. Those that survive acute myocardial infection may succumb later to congestive heart failure. Large fluid and protein losses from vomiting and diarrhea can cause severe dehydration and hypovolemic shock. Prolonged capillary refill time, tachycardia, hypotension, cool extremities, and low rectal temperature are signs of shock and hypoperfusion. Abdominal pain secondary to acute gastroenteritis or intussusception may be evident on palpation. Intestinal intussusceptions are a recognized complication of CPV infection.

Answer 206

The development of characteristic clinical signs in a dog at risk of infection often provides the first suspicion of CPV. Although considered a hallmark of CPV, leukopenia has been documented in less than 50% of infected dogs at the time of presentation. Leukopenia and neutropenia can reflect either marrow infection or sepsis and generally parallel the severity of clinical infection. An increase in circulating neutrophil counts often precedes clinical improvement. Anemia and hypoproteinemia, which can be a consequence of hypoalbuminemia, hypoglobulinemia, or both, can develop from enteric blood loss. Vomiting and diarrhea can contribute to electrolyte abnormalities, particularly hypokalemia, and dehydration leading to prerenal azotemia. Hypoglycemia can occur with sepsis. Prolonged APTT and PTT, low fibrinogen, and thrombocytopenia suggest DIC.

Answer 207

Administration of crystalloid fluids such as lactated Ringer's or 0.9% saline at volumes sufficient to restore and maintain hydration despite ongoing fluid losses is a key element of therapy. Supplementation of fluids with potassium and dextrose may be necessary to maintain normal serum potassium and glucose concentrations. Colloid administration (hetastarch or dextran 70) may be indicated for hypoproteinemia, especially if peripheral edema and/or effusion develop in third spaces. Plasma transfusion has been considered as an adjunctive treatment for hypoproteinemia but may not be as effective as nonprotein colloids because a large volume is required to achieve a small increase in plasma protein at the risk of fluid overload. Other considerations in the supportive care of affected dogs include control of persistent vomiting with antiemetic drugs such as metoclopramide, phenothiazine derivatives (chlorpromazine), serotonin antagonists (ondansetron), and NK-1 receptor antagonists (maropitant).

Answer 208

Canine distemper is caused by an enveloped single-stranded RNA virus in the Paramyxoviridae family and is closely related to viruses that cause measles, rinderpest, and distemper in other animals.

Answer 209

CDV is transmitted by oronasal exposure to virus-contaminated respiratory secretions, vomitus, feces, urine, and environmental fomites. CDV is also spread efficiently by inhalation of virus particles in respiratory aerosols generated by coughing and sneezing, as well as aerosols of other excretions. The incubation period typically ranges from 1 to 3 weeks. Virus shedding starts within 7 to 10 days of exposure during the preclinical incubation phase and can continue for 60 to 90 days. Dogs with subclinical infection also shed virus in feces. Thus, infected dogs may be contagious for up to 3 months.

Answer 210

CDV causes systemic infection of epithelial tissues in many organ systems. Following exposure, virus infects and replicates locally in macrophages and monocytes in the tonsils, upper respiratory tract epithelium, and regional lymph nodes, reaching peak virion production by 2 to 4 days after inoculation. Viremia occurs 4 to 6 days later, with spread of virus to the stomach, small intestine, spleen and hepatic macrophages, bone marrow, and other lymphoid sites. The widespread increase in virus production is associated with fever and lymphopenia. A second viremia follows within a few days and is responsible for infection of epithelial cells in multiple organs, including the eyes, skin, and central nervous system (CNS). Virus shedding from the respiratory, GI, and urogenital tracts coincides with epithelial infection. Virus persists for long periods of time in the uvea, uroepithelium, epidermis, and CNS;

Answer 211

Viral infection in bone marrow and other lymphoid tissues can result in profound and protracted immunosuppression, particularly young dogs, due to T cell depletion and other undefined mechanisms.

Answer 212

Dogs with poor immune responses develop viral infection of several additional tissues including skin and other glandular and epithelial organs. Such animals generally exhibit severe clinical signs and are likely to die as a result of infection. Those animals that do recover from the initial clinical signs maintain virus in tissues and are likely to subsequently develop clinical signs of CNS disease. In animals that mount an intermediate level of immune response, mild or clinically silent infection may develop, with virus persisting in the lungs, skin, or CNS. Such animals may undergo a complete recovery, or may develop signs of CNS disease. Animals that mount strong immune responses are unlikely to develop signs of systemic infection but may still develop signs of CNS disease.

Answer 213

The pathogenesis of neurologic disease in CDV-infected dogs is complex. Dogs, especially the young or immune-suppressed, may develop acute demyelination attributed to direct viral injury in the absence of inflammatory reactions.

Answer 214

Chronic encephalitis appears to be a consequence of inflammatory responses to viral antigens in CNS cells, with macrophage activation and release of cytotoxic mediators playing a role in destruction and demyelination of CNS cells.

Answer 215

Affected dogs may be lethargic, anorexic, dehydrated, and febrile, and they frequently have respiratory signs initially. These include serous or mucopurulent oculonasal discharge and cough. Viral infection of the lower respiratory tract results in pneumonia. Depending on viral strain, affected dogs may also have vomiting and mucoid or hemorrhagic diarrhea from viral replication in the GI epithelium. Virus infection of ocular tract epithelium can cause photophobia, anterior uveitis, and chorioretinitis. Recovered animals may have hyper-reflective retinal lesions that develop from retinal atrophy and scarring, as well as keratitis sicca from scarring of the lacrimal glands. Optic neuritis may cause blindness or mydriasis; blindness can also result from serous retinal detachments. Production of large amounts of virus occurs in uroepithelium, including the kidneys and lower urinary tract, which may cause clinical signs associated with kidney and bladder dysfunction. Viral infection of the epidermis can result in a pustular rash and hyperkeratosis or “hardening” of the nasal planum and footpads. Infection of developing enamel buds in young puppies prior to eruption of the permanent dentition results in enamel hypoplasia. Some dogs, especially young large-breed dogs, are susceptible to metaphyseal osteosclerosis of long bones, which is typically not associated with lameness. Neurologic signs may develop starting 1 to 3 weeks after recovery from systemic signs or can develop months later. Neurologic signs can develop in dogs that had no evidence of systemic disease. Neurologic abnormalities can reflect lesions in any CNS site and include seizures, ataxia, hypermetria, paraparesis or tetraparesis, and severe cervical pain. Myoclonus, either generalized or focal, is a common clinical sign and is strongly suggestive of CDV infection. Abortion and neonatal death have been seen.

Answer 216

Largely supportive. Animals with secondary bacterial bronchopneumonia or other infections are candidates for antibiotics. Seizure control with diazepam, pentobarbital, or potassium bromide may be necessary.

Answer 217

Canine adenovirus type 1 (CAV-1), a nonenveloped double-stranded DNA virus in the Adenoviridae family, is the cause of infectious canine hepatitis (ICH). CAV-1 is closely related genetically and antigenically to CAV-2. In addition to the domestic dog, CAV-1 also infects wolves, coyotes, foxes, bears, and marine mammals.

Answer 218

Oronasal exposure to virus-contaminated body secretions and excretions and environmental fomites. The incubation period is 4 to 9 days. Virus shedding occurs during acute infection in all body secretions (saliva, respiratory) and excretions (feces, urine) and is shed in urine for up to 6 to 9 months. The virus is relatively hardy, surviving in the environment for days to months, and is resistant to most disinfectants

Answer 219

CAV-1 causes systemic infection with tropism for endothelial cells, epithelial cells, and hepatocytes. After exposure, CAV-1 replicates in lymphoid tissue of the tonsils and regional lymph nodes. Viremia follows, leading to infection of other tissues.

Answer 220

Direct cytopathic effects of the virus in the liver, eyes, and kidney contribute to early clinical signs, which can become apparent in naïve dogs 4 to 9 days after exposure.

Answer 221

The extent of hepatic necrosis is a function of the level of antiviral antibody present at the time of infection: Animals with minimal antibody exhibit extensive necrosis that is often fatal; those with high levels of antibody exhibit minimal clinical signs; and those with intermediate antibody levels are susceptible to persistent hepatic inflammation..

Answer 222

Clinical signs of anterior uveitis (“blue eye”) initially develop as a consequence of the inflammation following infection of corneal endothelial cells and the deposition of immune complexes as antibody responses to the virus increase.

Answer 223

Initial clinical signs include fever, depression, and lethargy. Later, development of abdominal discomfort, mucous membrane pallor, and inflammation of the tonsils and pharynx with tonsillar and cervical lymph node enlargement occur. Abdominal fluid and hepatomegaly will be detected in some dogs. Laryngitis, tracheitis, pneumonia, coughing, vomiting, and diarrhea occur in some. In severe cases, petechial and ecchymotic hemorrhages and epistaxis may develop from coagulation abnormalities secondary to hepatic dysfunction and DIC. Icterus is uncommon despite the presence of hepatic necrosis. Neurologic signs may be seen as a consequence of hepatic encephalopathy or CNS infection; measurement of bile acids or plasma ammonia concentrations, if elevated, would support hepatic encephalopathy as a cause of neurologic signs. Dogs with severe disease may die within hours of showing clinical signs, whereas dogs with less severe disease may exhibit clinical improvement 5 to 7 days after onset of clinical signs. Anterior uveitis and glomerulonephritis from deposition of immune complexes may occur within a month of recovery.

Answer 224

Supportive care Intravenous fluid therapy to replace losses from vomiting or diarrhea Administration of blood products to manage the complications of hemorrhage and DIC. In patients with neurologic signs from hepatic encephalopathy, administration of lactulose via enema (or orally if the patient is not vomiting) can help reduce circulating concentrations of encephalotoxins.

Answer 225

Canine adenovirus type 2 (CAV-2) is a nonenveloped double-stranded DNA virus in the Adenoviridae family that is genetically and antigenically related to CAV-1. CAV-1 and CAV-2 share the same host range. Canine parainfluenza virus (CPiV) is an enveloped single-stranded RNA virus in the Paramyxoviridae family. CAV-2 and CPiV are part of a complex of pathogens causing canine infectious respiratory disease (CIRD) or “kennel cough.”

Answer 226

Both viruses are transmitted by oronasal exposure through direct contact with virus-contaminated respiratory secretions and environmental fomites, as well as inhalation of aerosolized respiratory droplets generated by sneezing or coughing. The incubation period ranges from 3 to 10 days, and virus shedding in respiratory secretions generally ceases within 10 days. CAV-2 is relatively hardy and can survive in the environment for days to months, but CPiV is fragile and survives for only a short period outside of the host.

Answer 227

PATHOGENESIS Virus replication occurs in nonciliated epithelial cells of the upper respiratory tract and type 2 alveolar cells in the lower respiratory tract, causing epithelial destruction and inflammation. Peak replication occurs between days 3 and 6 postinfection and rapidly declines thereafter. Dogs can be asymptomatic or have mild clinical disease consisting of rhinitis, tracheitis, and bronchitis. However, damage and disruption of the epithelial barrier predisposes to infection with other viral and bacterial respiratory tract pathogens. Coinfections can increase tissue damage and worsen clinical disease, including progression to pneumonia. There is one report of fatal neurologic disease in puppies due to CAV-2 infection.

Answer 228

Canine influenza A subtype H3N8 is an enveloped single-strand RNA virus in the family Orthomyxoviridae. Interspecies transmission of equine influenza A H3N8 viruses from horses to dogs at some point prior to 2004. Canine influenza H3N8 virus (CIV) Viral adaptation to the dog has resulted in a canine-specific pathogen that replicates efficiently in the respiratory tract to cause clinical disease and is sustained in canine populations by dog-to-dog transmission

Answer 229

CIRD or “kennel cough.”

Answer 230

Canine influenza is a highly contagious respiratory infection, and outbreaks reach epidemic proportions in facilities with high density and high-turnover populations. Transmission is by oronasal contact with infected dogs or contaminated fomites, and by inhalation of aerosols generated by coughing and sneezing

Answer 231

Because CIV is still a novel virus for most dogs, virtually all exposed dogs become infected and about 80% develop clinical disease nfluenza virus replicates in mucosal epithelial cells lining the airways from the nose to the terminal airways, in bronchiole gland epithelium, and in pulmonary macrophages. Viral replication causes epithelial cell necrosis and destruction of the respiratory epithelial barrier, predisposing to secondary infections by a variety of commensal bacteria, including Streptococcus spp., Staphyloccocus spp., Escherichia coli, Klebsiella, Pasteurella multocida, and Mycoplasma spp. The primary viral infection initiates intense neutrophilic and monocytic inflammatory responses resulting in rhinitis, tracheitis, bronchitis, and bronchiolitis.

Answer 232

Canine respiratory coronavirus (CRCoV) is an enveloped single-strand RNA virus in the Coronaviridae family. CRCoV is a group 2 coronavirus that is genetically related to the bovine and human coronaviruses associated with respiratory infections in cattle and humans, respectively. CRCoV is genetically and antigenically distinct from group 1 canine enteric and pancytotropic coronaviruses. CRCoV can cause acute respiratory infection and is part of the complex of viruses and bacteria associated with CIRD or “kennel cough.”[68]

Answer 233

Canine enteric coronavirus (CECoV), an enveloped single-stranded RNA virus in the family Coronaviridae, is a group 1 coronavirus that is genetically and antigenically distinct from the group 2 coronavirus, canine respiratory coronavirus (CRCoV). CECoV can infect many species of canids and is considered prevalent in dogs from group-housing facilities such as kennels and shelters. CECoV is spread primarily by the fecal-oral route to susceptible dogs

Answer 234

CECoV infects epithelial cells in the villus tips of the small intestine. A malabsorptive diarrhea results as a consequence of loss of villus surface area. The development of a local intestinal immune response terminates clinical signs and ultimately viral shedding.

Answer 235

CECoV can be found in feces of clinically normal dogs. Diarrhea (occasionally with blood) is the principle sign in clinically affected dogs. Vomiting may be seen before or after diarrhea in some animals. Anorexia and lethargy are common features, and if vomiting and diarrhea are severe, dehydration may ensue. Clinical disease from CECoV is considered infrequent compared with other viral enteropathies and is usually more severe in neonatal animals, with diminishing severity of clinical disease in older animals. Clinical signs abate after 7 to 10 days in most dogs, but the clinical course may be longer in dogs that develop secondary complications or infections.

Answer 236

A novel group 1 coronavirus isolate related to CECoV has been identified as a cause of severe clinical disease in puppies and juvenile dogs. The key pathophysiologic feature of this coronavirus is tropism for a wide variety of cell types. The viral features accounting for the expanded cell tropism have yet to be defined but are suspected to reflect a mutation. Pancytotropic CCoV antigen and RNA have been identified in lungs, kidneys, liver, spleen, GI tract, lymph nodes, and RNA in the brain.

Answer 237

Compared with other enteric viruses, clinical disease caused by canine rotavirus appears to be uncommon. Canine rotavirus can cause subclinical or mild gastroenteritis in puppies younger than 3 months old. Severe fatal enteritis has been reported in puppies younger than 2 weeks old. There is a high seroprevalence in adult dogs. Although rotaviruses are generally species-specific, genetic sequence analyses have suggested the possibility of transmission of canine rotaviral isolates to people. Infection usually occurs via oronasal exposure to virus-contaminated feces or fomites. Rotaviruses are durable in the environment.

Answer 238

After exposure, rotavirus infects epithelial cells of the villus tip of the jejunum and ileum. Loss of villus epithelial cells ensues with development of villus atrophy. Virus is shed early as infected, necrotic epithelial cells are sloughed from the villus. Anorexia, vomiting, and mild diarrhea, which can occasionally be bloody, are the typical clinical signs of rotaviral gastroenteritis. Recovery is expected in most animals within 5 to 7 days of onset of clinical signs.

Answer 239

Canine herpesvirus (CHV) is an enveloped, double-stranded DNA virus in the Herpesviridae family. The host range is restricted to domestic and wild canids. Although controversial and not clearly defined, CHV is considered part of a complex of pathogens causing CIRD or “kennel cough.” It may have a secondary role, with activation of viral replication induced by infection by more virulent respiratory pathogens. Genetically related to feline and equine herpesvirus. The virus is transmitted by oronasal contact with infectious respiratory or genital secretions and may also occur transplacentally. The

Answer 240

Transplacental infection during primary infection of pregnant dogs results in fetal resorption, abortion, stillbirths, or birth of weak puppies that die within days. Immunity following primary infection protects future litters. Infection of naïve puppies younger than 2 weeks old causes fatal generalized necrotizing and hemorrhagic disease. Neonatal puppies are infected by oronasal contact with infectious birth canal secretions in dams with actively replicating virus, or via grooming by the dam.

Answer 241

CHV first replicates in the epithelial cells of the oropharynx and tonsils. Virus subsequently enters macrophages, which allows spread to other tissues hematogenously, including the lymph nodes, spleen, adrenal glands, kidneys, lungs, liver, and CNS. T he lower body temperature of neonates, in conjunction with a limited capacity to mount a febrile response, facilitates systemic spread of the virus. Infection of older pups and adults is confined to the respiratory, ocular, or genital tract without systemic spread. Most infections are asymptomatic or may present as a mild and self-limiting respiratory, ocular, or genital disease.

Answer 242

Following a short replication period, CHV establishes latent infection in neurons of the trigeminal and lumbosacral ganglia, lymphocytes in the retropharyngeal lymph nodes and tonsils, and epithelial cells in the parotid salivary gland. Reactivation of viral replication can be provoked by stress and immunosuppressive disease or therapy.

Answer 243

Infected neonatal puppies exhibit persistent crying, anorexia, abdominal pain, dyspnea, and petechial hemorrhages 1 to 3 days before death. Most puppies in affected litters die between 1 and 4 weeks postpartum. Petechial hemorrhages in the liver, kidneys, and lungs are typical lesions observed on necropsy. Older puppies develop mild signs of respiratory disease (rhinitis, pharyngitis) with spontaneous recovery, but latent infections may emerge later as a cause of neurologic disease, with signs of ataxia, blindness, or central vestibular disease most common. Infection in adult dogs is usually asymptomatic, but some dogs have rhinitis, pharyngitis, vaginal or preputial hyperemia, hyperplasia of vaginal mucosal lymphoid follicles, and sometimes submucosal hemorrhages. Corneal ulceration has been reported in adult dogs during natural infection with CHV, while conjunctivitis occurred in experimentally infected dogs. The clinical significance of CHV infections in ocular diseases is not defined, but CHV should be considered a potential cause of conjunctivitis or corneal disease after more common causes have been excluded.

Answer 244

Young dogs are clinically affected more frequently than older animals. The primary clinical sign of COPV infection is the appearance of papillomas, or warts, in the oral cavity or other epithelial sites. Papillomas typically regress within 4 to 8 weeks (and occasionally longer) when cell-mediated immune responses cause T-cell infiltration into the wart COPV infection causes oral, ocular, and cutaneous papillomas. Oral papillomas typically occur in dogs younger than 2 years of age, ocular papillomas occur in dogs 6 months to 4 years of age, and cutaneous papillomas occur in older dogs. CfPV-2 causes lesions on footpads and interdigital spaces of the feet of adult dogs and immunosuppressed dogs. The lesions associated with this virus were more endophytic (inward growing) than exophytic (outward growing) and persisted for much longer periods of time. In addition, CfPV-2 has been associated with the development of squamous cell carcinomas (SCC) in immunosuppressed dogs. This virus may also play a role in the development of pigmented cutaneous papillomatosis

Answer 245

Humoral immune responses, although capable of preventing infection, do not seem to play a role in regression of lesions

Answer 246

RV is spread primarily by inoculation of a naïve animal with infected saliva; thus bite wounds are the most common mode of RV transmission. The incubation period is variable and dependent on size of the viral inoculum, extent of nerve supply to injured tissue, distance from the site of inoculation to the spinal cord, and host factors such as age and immune responses. Virus can be shed in the saliva for almost 2 weeks before clinical signs develop.

Answer 247

Following inoculation, virus replicates in local tissue then enters nerve endings through neuromuscular junctions or breaches in the axonal sheath of injured nerve fibers. Virus spreads along axons in the peripheral nerves to the CNS. Once in the CNS, virus spreads among adjacent axons to involve more neurons, spreading rapidly to the brainstem and then forebrain.

Answer 248

While replicating in the CNS, virus exits the CNS along peripheral nerve fibers to enter other tissues, including salivary glands. Thus, virus in saliva reflects CNS infection.

Answer 249

1. Clinical signs often start with a prodromal phase of 2 to 3 days’ duration that is characterized by nervousness, anxiety, or other behavior changes. There may be paresthesia at the site of inoculation. 2. As clinical signs progress, forebrain signs of irritability, restlessness, pica, photophobia, and hyperesthesia may be apparent. These clinical signs are often referred to as the furious form of rabies and can progress to incoordination, seizures, and death. 3. Paralytic, or dumb, forms of rabies are characterized by lower motor neuron disease beginning in the area of initial injury and eventually involving the entire CNS. 4. Dysphagia from paralysis of the muscles of deglutition causes accumulation of saliva in the oral cavity, which can be a source of infection to owners and veterinarians attending to such patients. Once clinical signs have developed, death typically follows within 10 days as the animal develops coma and respiratory paralysis.

Answer 250

Pseudorabies is an uncommon but fatal disease of dogs caused by an enveloped, double-stranded DNA virus in the alpha-herpesvirus family. Affected dogs usually have a history of having been in contact with pigs, the primary virus reservoir that causes “mad itch.” TRANSMISSION Most cases in dogs are believed to result from ingestion of infected raw pork. The incubation period is 3 to 6 days. Despite the presence of an envelope, pseudorabies virus is relatively stable in the environment. PATHOGENESIS After ingestion, the virus enters nerve endings in the mucosa and spreads to the brain along nerve axons. Inflammation and functional abnormalities in brain cells result in signs. CLINICAL SIGNS Signs of neurologic dysfunction are common features of the disease. Neurologic abnormalities can be variable and have included ataxia, abnormal pupillary light responses, restlessness, trismus, and cervical rigidity. Ptyalism, tachypnea, and hyperpnea are common. Intense pruritus of the head and neck area can lead to self-induced excoriation. In some dogs, vomiting and diarrhea predominate. The clinical course of pseudorabies infection in dogs is usually swift, with most dogs dying within 48 hours after onset of neurologic signs.

Answer 251

WNV is a nonenveloped, single-stranded RNA virus in the family Flaviviridae. WNV is found worldwide and is maintained in natural settings via transmission from infected to naïve birds via mosquitoes. Mosquitoes are able to transmit the virus to dogs. Experimental infection has shown that dogs are able to develop viremia, which is typically of low magnitude and of short duration.Despite being able to support viremia, clinical disease in dogs either naturally exposed, or experimentally infected, is uncommon, even in dogs pretreated with large doses of glucocorticoids. Signs of CNS disease, reflecting meningoencephalitis, and fever have been most consistently observed in naturally infected dogs; multisystemic disease has also been reported. Reports in dogs suggest that the organs most likely to have virus are the brain, kidney, and heart

Answer 252

The bornavirus (BV) is an enveloped, single-stranded RNA virus in the family Bornaviridae. BV causes a fatal disease of the CNS in horses and other animals. Clinical disease in dogs appears to be relatively uncommon, and seropositivity in the absence of clinical signs appears possible. The pathogenesis of the disease in dogs is unknown, but clinical signs in dogs have included tremors, salivation, mydriasis, and circling. The infection is suspected based on the histopathologic observation of nonsuppurative encephalomyelitis predominantly in gray matter of the brain. Demonstration of viral RNA by in situ hybridization or PCR-based assays has provided definitive diagnosis.

Answer 253

Systemic mycoses are fungal infections that disseminate from a single portal of entry. The respiratory system serves as the portal of entry for most systemic fungi that affect dogs and cats, but entry may occur via the gastrointestinal (GI) system or skin. Immune suppression, while playing a major role in the development of systemic mycoses in humans, does not appear to play as significant a role in animals. Systemic fungal infections cause disease, the clinical signs of which are dependent on which body systems are involved

Answer 254

Weight loss, lymphadenopathy, and fever are typical of most systemic mycoses. Because the respiratory system is the usual portal of entry, clinical signs such as cough, dyspnea, and exercise intolerance are common. If the GI system is the portal of entry, as may occur with histoplasmosis, malabsorption may lead to severe diarrhea and weight loss.

Answer 255

The principal antifungal agents are antibiotics produced by microorganisms (e.g., amphotericin B, griseofulvin) and synthetic agents (e.g., potassium iodide, flucytosine, azole derivatives, allylamine derivatives, chitin synthase inhibitors). Pharmacologic principles of antifungal therapy are only partially understood; in vitro testing of fungi for resistance to antifungal agents provides information of variable clinical usefulness; susceptibility testing yields variable results; and tissue distribution of antifungal agents correlates variably with the clinical outcome.

Answer 256

Blastomycosis is a systemic fungal infection that usually originates in the lungs and then disseminates to the lymphatics, skin, eyes, bones, and other organs. The dog is most commonly affected.Blastomycosis is not a contagious disease. It follows contact with the organism in the environment. Infection usually occurs via a respiratory route after the host inhales infective conidiophores. Hematogenous and lymphatic dissemination results in multisystemic pyogranulomatous disease. Although dissemination can be to any organ system, the lymph nodes, eyes, skin, bones, subcutaneous tissues, and prostate are organs commonly affected in dogs. skin, subcutaneous tissues, eyes, CNS, and lymph nodes are most commonly affected in cats. The immune response determines the severity of clinical disease, but blastomycosis is not considered an opportunistic infection. Antibody production occurs in most, but not all, cases, with the highest titers usually found in dogs with severe disseminated disease. Recovery from infection is dependent on cell-mediated immunity

Answer 257

Clinical findings in animals with blastomycosis vary greatly because of the multisystemic nature of the disease. One or more organ systems may be involved. Nonspecific signs such as anorexia, depression, weight loss, cachexia, and fever are commonBecause the lungs serve as the portal of entry for the Blastomyces organism, it is not surprising that pulmonary signs are seen in 65% to 85% of affected dogs. Diffuse lymphadenopathy is seen in about 40% to 60% of dogs with blastomycosis. Cutaneous signs. Ocular involvement. Lameness caused by fungal osteomyelitis or painful paronychia. The reproductive system is affected in approximately 5% to 10% of affected dogs. The nervous system is affected in less than 5% of affected dogs but is common in cats.

Answer 258

Lungs, GI tract

Answer 259

Histoplasmosis occurs most commonly in cats and dogs younger than 4 years of age. Dogs: The clinical findings are related to the route of infection and the extent of systemic dissemination. Clinically inapparent infection is probably common after inhalation of organisms. In those dogs showing clinical signs, findings vary greatly, but GI signs are most common Cats: Depression, anorexia, fever, pale mucous membranes, and weight loss are common. Pulmonary involvement. Cough is uncommon. Hepatomegaly, splenomegaly, or lymphadenopathy is noted in about a third of affected cats. Ocular involvement. Fungal osteomyelitis may cause lameness in one or more limbs. Cutaneous lesions consisting of multiple small nodules that may ulcerate and drain or crust over are noted less commonly than in animals affected with blastomycosis. GI signs other than anorexia are uncommon in cats with histoplasmosis when compared to dogs. Oral and lingual ulceration has been reported as an unusual manifestation. Icterus is occasionally seen in cats with hepatic involvement.

Answer 260

Cryptococcosis is an opportunistic systemic fungal infection of worldwide significance that usually initially infects the nasal cavity, paranasal tissues, or lungs. It can then disseminate, most commonly to the skin, eyes, or CNS. Among domestic animals, it occurs most commonly in the cat, in which it is the most common of the systemic mycoses. Unlike the other systemic mycoses, cryptococcosis does not follow strict geographic boundaries but is most common in the southeastern and southwestern United States, Southern California, the western part of British Columbia, and the east coast of Australia. Cryptococcosis is caused by saprophytic, round, yeastlike organisms with a restricted ecologic niche. Cryptococcus is considered infectious as a desiccated yeast cell or basidiospore in the environment that enters the body primarily through the respiratory system, where it infects nasal, paranasal, or lung tissue before disseminating more widely with a predilection for the CNS.

Answer 261

Cryptococcosis is not a contagious disease. Infection occurs most commonly via inhalation of yeast from the environment. Most yeasts are probably too large to be inhaled into the lungs and settle out in the nasal cavity or nasopharynx, where they can produce disease or result in animals becoming asymptomatic carriers of the organism. Direct extension from the nasal cavity through the cribriform plate to the CNS or to the paranasal soft tissues and skin is common. Although dissemination can be to any organ system, the skin, eyes, and CNS are most commonly affected. Lesions consist of either granulomatous inflammation with few organisms or gelatinous masses of organisms with little inflammation.

Answer 262

As with the other systemic mycoses, the immune response determines the severity of clinical disease. Antibodies are readily produced by the humoral immune system but are not considered protective. Recovery, therefore, is dependent on cell-mediated immunity. Cryptococcus spp. appears to be a primary pathogen of immunocompetent cats and dogs. An association with feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV) infections in cats has been reported, and chronic glucocorticoid use has been implicated as a predisposing factor in both cats and dogs

Answer 263

Usually related to upper respiratory, nasopharyngeal, cutaneous, ocular, or CNS involvement. Unlike in other systemic mycoses, the lungs are not commonly clinically affected. Nonspecific signs such as depression and anorexia are common in chronic cases, but fever is uncommon. Upper respiratory signs associated with nasal cavity involvement are seen in 50% to 80% of affected cats. The skin or subcutaneous tissues are affected in approximately 40% to 50% of infected cats. The eyes are affected in 20% to 25% of infected cats, especially those with CNS involvement. Canine cryptococcosis is typically seen in dogs younger than 4 years of age. CNS involvement is reported in approximately 50% to 80% of affected dogs. The brain is affected in most of these dogs. Signs of nervous system involvement may include mental depression, vestibular syndrome, ataxia, cranial nerve deficits (especially cranial nerves V, VII, and VIII), seizures, paresis, blindness, hypermetria, and cervical pain. In dogs with CNS signs, other systems are usually affected as well, reflecting multisystemic dissemination. The upper respiratory system or paranasal tissues are affected in approximately 50% of dogs with cryptococcosis

Answer 264

Unique among the continents, North America is host to three of the geographically defined major endemic mycoses: histoplasmosis, blastomycosis, and coccidioidomycosis. Histoplasma capsulatum and Blastomyces dermatitidis convert in vivo into a “yeast form”; Coccidioides immitis converts to a “spherule.” Infection in mammals occurs most commonly by inhalation of airborne spores. Inhaled saprophytic spores cannot be killed by neutrophils and are small enough (3 to 5 µm) to lodge in host alveoli. Recovery from infection depends on the competence of the host's cell-mediated immunity. Compromised cell-mediated immunity, due to genetics, chemotherapy for neoplasia, organ transplant, or immune-mediated disease, or as a consequence of immunocompromising viral infection renders the host less able to resist colonization and dissemination of these fungi

Answer 265

Aspergillosis: Aspergillus species are filamentous fungi that are ubiquitous under appropriate environmental conditions and not typically infectious due to host resistance. Pets acquire infectious aspergillosis in two forms: (1) localized (usually sinonasal) and (2) disseminated (involving two or more noncontiguous organs), both are more common in the dog than cat. Aspergillus species typically proliferate by producing spores in vegetative decaying soil and water

Answer 266

Canine sinonasal aspergillosis is characterized by colonization and invasion of the nasal passages and frontal sinuses by the saprophytic fungus, Aspergillus fumigatus. A. fumigatus is regarded as an opportunistic pathogen, suggesting that some preexisting local nasal mucosal immunocompetence allowed its establishment in the upper respiratory tract. Sinonasal aspergillosis may occur as an opportunistic primary infection or it may occur secondary to the presence of a foreign body (foxtail, splinter), nasal trauma, or neoplasia. The disease primarily affects young to middle-aged mesaticephalic and dolichocephalic breeds and is progressive unless effective specific therapy is given. German Shepherds and Rottweilers are the pure breeds more commonly affected, but nasal aspergillosis occurs in mixed-breed dogs as well.

Answer 267

Colonization and invasion of the nasal mucosa by A. fumigatus results in destruction and necrosis of the nasal turbinates, often accompanied by frontal sinus osteomyelitis. The cribriform plate, palatine bones, and orbit are sometimes involved.

Answer 268

Facial pain, anorexia, sneezing, and copious mucoid to hemorrhagic nasal discharge and crusting are common clinical signs. Life-threatening epistaxis can occur secondary to erosion of the nasal vasculature. With chronicity, depigmentation, and ulceration of the nares and masticatory muscle atrophy result. CNS involvement (encephalitis, meningitis) precipitating seizures can result after erosion of the cribriform plate.

Answer 269

Disseminated aspergillosis is most commonly diagnosed in dogs and cats that are terminally ill from the disease. Disseminated aspergillosis typically involves multiple organ systems with no history of nasal or pulmonary involvement. Aspergillus terreus, A. deflectus, A. flavipes, and rarely A. fumigatus have been reported in cases where the species has been identified. Disseminated aspergillosis is believed to occur after inhalation of small spores (s dextrose agar. Serology is not reliable (false negatives have been reported). The prognosis for recovery is poor despite aggressive antifungal therapy and supportive care. Intravenous amphotericin B, itraconazole, fluconazole, or voriconazole are advised initially. Long-term (sometimes for life) oral azole therapy can be attempted if an initial positive response to intravenous antimycotic drug administration occurs.

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