Avian malaria in African black-footed penguins

Ten captive-reared African black-footed penguins (Spheniscus demersus) from a large outdoor colony were monitored for avian malaria, using several diagnostic tests. One treatment regimen was evaluated. Thin smear blood evaluation enabled detection of seven parasitemias involving Plasmodium relictum and Plasmodium elongatum in the penguins. Leukocytosis (relative lymphocytosis) was characteristic of infected birds. Parasitemia was detected as early as 21 days prior to onset of clinical signs (depression, anorexia, regurgitation, pale mucous membranes, and respiratory distress). The single bird that died had clinical signs only a few hours prior to its death. Treatment consisted of 0.03 mg of primaquine phosphate base/kg body weight, administered orally once daily for 3 days. Oral chloroquine phosphate therapy, given simultaneously, was administered in an initial loading dose of 10 mg of chloroquine phosphate base/kg body weight, followed by doses of 5 mg/kg at 6, 18 and 24 hours after the initial chloroquine dose. This treatment regimen prevented mortality and cleared parasites from the blood. Recurrences of malaria occurred in two birds that had received this treatment.     

Plasmodium Juxtanucleare associated with mortality in black-footed penguins (Spheniscus demersus) admitted to a rehabilitation center.

Five black-footed penguins (Spheniscus demersus) admitted to the Southern African Foundation for the Conservation of Coastal Birds, in Cape Town, South Africa, died from malaria infection. Evidence for malaria as the cause of death included antemortem clinical signs, parasitemia, splenomegaly, pulmonary edema, and the presence of histologically visible schizonts in the reticuloendothelial system. A portion of the malarial small subunit ribosomal ribonucleic acid gene was detected by polymerase chain reaction from postmortem blood samples from all the birds. A species-specific variable region of this gene was compared with the same region on genes from other known avian malarial organisms, establishing that Plasmodium juxtanucleare was involved.     

Neurotropism of highly pathogenic avian influenza virus A/chicken/Indonesia/2003 (H5N1) in experimentally infected pigeons (Columbia livia f. domestica)

This investigation assessed the susceptibility of experimentally infected pigeons to the highly pathogenic avian influenza virus (HPAIV) H5N1 that caused recent outbreaks of avian influenza in birds and humans in several countries of Asia. For this purpose 14 pigeons were infected ocularly and nasally with 10(8) EID50 and clinical signs were recorded and compared with five chickens infected simultaneously as positive controls. The chickens demonstrated anorexia, depression, and 100% mortality within 2 days postinoculation. Three of the pigeons died after a history of depression and severe neurological signs consisting of paresis to paralysis, mild enteric hemorrhage, resulting in a mortality of 21%. Gross lesions in these pigeons were mild and inconsistent. Occasionally subcutaneous hyperemia and hemorrhage and cerebral malacia were observed. Microscopic lesions and detection of viral antigen were confined to the central nervous system of these pigeons. In the cerebrum and to a minor extent in the brain stem a lymphohistiocytic meningoencephalitis with disseminated neuronal and glial cell necrosis, perivascular cuffing, glial nodules, and in one bird focally extensive liquefactive necrosis could be observed. The remaining nine pigeons showed neither clinical signs nor gross or histological lesions associated with avian influenza, although seroconversion against H5 indicated that they had been infected. These results confirm that pigeons are susceptible to HPAIV A/chicken/Indonesia/2003 (H5N1) and that the disease is associated with the neurotropism of this virus. Although sentinel chickens and most pigeons did not develop disease, further experiments have to elucidate whether or not Columbiformes are involved in transmission and spread of highly pathogenic avian influenza.     

Infection with Mycobacterium simiae complex in four captive Micronesian kingfishers

CASE DESCRIPTION: 4 captive adult Micronesian kingfishers (Halcyon cinnamomina cinnamomina) at 3 zoologic institutions were examined routinely or because of dyspnea or lethargy. CLINICAL FINDINGS: All birds had marked hepatomegaly. Two birds had dyspnea caused by compression of air sacs by the enlarged liver, and 1 bird had generalized weakness and lethargy. Three birds had distended coelomic cavities, and 3 birds were thin or had lost weight. There were no consistent abnormalities in blood analytes. Results of most ancillary diagnostic tests such as acid-fast staining of cloacal or fecal swab specimens and culture of feces for acid-fast bacteria were negative. Results of examination of hepatic biopsy specimens in 2 of 4 birds were suggestive of mycobacteriosis. TREATMENT AND OUTCOME: 3 birds died or were euthanized soon after diagnosis. One kingfisher was isolated and monitored for 4 months without treatment and died during anesthesia for disease monitoring. Postmortem histologic examination revealed histiocytic hepatitis and acid-fast bacteria in all 4 birds. Bacteriologic culture of liver specimens yielded Mycobacterium simiae complex in all 4 birds. CLINICAL RELEVANCE: Infection with M simiae complex should be considered in ill Micronesian kingfishers, and further monitoring is warranted to determine whether this is an emerging pathogen in this species.     

Cardiovascular involvement in 8 dogs with blastomyces dermatitidis infection

BACKGROUND: Blastomycosis is a common systemic fungal infection in dogs. HYPOTHESIS: Dogs with cardiovascular involvement may have abnormalities in electrical conduction and valvular function, and may have a worse prognosis. ANIMALS: Eight client-owned animals. METHODS: Dogs with cardiovascular lesions caused by blastomycosis were identified from retrospective evaluation of medical records. RESULTS: Five dogs had de novo infections and 3 had recurrences of previously treated infections. Harsh labored breathing, lethargy, and anorexia were the most common historic complaints. Three dogs had syncope. Physical examination and clinicopathologic data were typical of blastomycosis and included dyspnea, increased lung sounds, and lethargy. In addition, 3 dogs had heart murmurs and 1 had a third-degree atrioventricular block. Four dogs had myocarditis and 2 had pericarditis or epicarditis. Two dogs had cardiac signs attributed to extracardiac compression by fungal granulomas and clinical signs were relieved by treatment. Half of the remaining 6 dogs were euthanized; 2 of these were not treated. Of the remaining 3 dogs, 1 dog died acutely while sleeping; the second died intraoperatively during an attempt to place an epicardial pacemaker; and the third had Blastomyces-induced endocarditis and died of heart failure. CONCLUSIONS AND CLINICAL IMPORTANCE: Blastomycosis should be considered in the differential diagnosis of dogs from endemic areas with inflammatory myocarditis, heart block, heart base or intracardiac mass lesions, syncope, or endocarditis.     

An outbreak of avian malaria in captive yellowheads/mohua (Mohoua ochrocephala)

CASE HISTORY: Eight mohua, or yellowheads (Mohoua ochrocephala), were held in a large open aviary over the summer months of 2003-2004, following their capture for captive breeding purposes. Two birds died of transportation trauma shortly after arrival, one became ill and died a month later, and another four died within a 2-week period in February 2004. The eighth bird also became ill at this time but survived for a year following treatment with chloroquine and doxycycline. CLINICAL AND PATHOLOGICAL FINDINGS: The affected birds were depressed, lethargic and dyspnoeic. Necropsy of three birds showed a slightly pale and swollen liver and spleen. Impression smears of the liver of one bird revealed schizonts resembling Plasmodium spp. within the cytoplasm of many hepatocytes, which was confirmed histopathologically. Similar protozoal organisms were seen within splenic histiocytes and pulmonary endothelial cells of 5/6 birds. Electron microscopy identified these as protozoal schizonts containing merozoites of similar size and structure to those of Plasmodium spp. DIAGNOSIS: The birds were infected with a protozoal haemoparasite resembling Plasmodium spp.; asexual stages within hepatocytes and endothelial cells of the lung and spleen were typical of this organism. CONCLUSIONS AND CLINICAL RELEVANCE: The mohua captured from west Otago were highly susceptible to avian malaria as they came from an isolated population that was likely to be na?ve and have had no previous contact with this organism. The birds were probably infected by bites from mosquitoes feeding off local populations of blackbirds subsequently found to be infected with Plasmodium spp.     

Experimental West Nile virus infection in Eastern Screech Owls (Megascops asio)

Eastern Screech Owls (EASOs) were experimentally infected with the pathogenic New York 1999 strain of West Nile virus (WNV) by subcutaneous injection or per os. Two of nine subcutaneously inoculated birds died or were euthanatized on 8 or 9 days postinfection (DPI) after <24 hr of lethargy and recumbency. All subcutaneously inoculated birds developed levels of viremia that are likely infectious to mosquitoes, with peak viremia levels ranging from 10(5.0) to 10(9.6) plaque-forming units/ml. Despite the viremia, the remaining seven birds did not display signs of illness. All birds alive beyond 5 DPI seroconverted, although the morbid birds demonstrated significantly lower antibody titers than the clinically normal birds. Cagemates of infected birds did not become infected. One of five orally exposed EASOs became viremic and seroconverted, whereas WNV infection in the remaining four birds was not evident. All infected birds shed virus via the oral and cloacal route. Early during infection, WNV targeted skin, spleen, esophagus, and skeletal muscle. The two morbid owls had myocardial and skeletal muscle necrosis and mild encephalitis and nephritis, whereas some of the clinically healthy birds that were sacrificed on 14 DPI had myocardial arteritis and renal phlebitis. WNV is a significant pathogen of EASOs, causing pathologic lesions with varying clinical outcomes.     

An outbreak of avian malaria in captive yellowheads/mohua (Mohoua ochrocephala)

CASE HISTORY: Eight mohua, or yellowheads (Mohoua ochrocephala), were held in a large open aviary over the summer months of 2003–2004, following their capture for captivebreeding purposes. Two birds died of transportation trauma shortly after arrival, one became ill and died a month later, and another four died within a 2-week period in February 2004. The eighth bird also became ill at this time but survived for a year following treatment with chloroquine and doxycycline.

CLINICAL AND PATHOLOGICAL FINDINGS: The affected birds were depressed, lethargic and dyspnoeic. Necropsy of three birds showed a slightly pale and swollen liver and spleen. Impression smears of the liver of one bird revealed schizonts resembling Plasmodium spp. within the cytoplasm of many hepatocytes, which was confirmed histopathologically. Similar protozoal organisms were seen within splenic histiocytes and pulmonary endothelial cells of 5/6 birds. Electron microscopy identified these as protozoal schizonts containing merozoites of similar size and structure to those of Plasmodium spp.

DIAGNOSIS: The birds were infected with a protozoal haemoparasite resembling Plasmodium spp.; asexual stages within hepatocytes and endothelial cells of the lung and spleen were typical of this organism.

CONCLUSIONS AND CLINICAL RELEVANCE: The mohua captured from west Otago were highly susceptible to avian malaria as they came from an isolated population that was likely to be naïve and have had no previous contact with this organism. The birds were probably infected by bites from mosquitoes feeding off local populations of blackbirds subsequently found to be infected with Plasmodium spp.     

Host response in rabbits to infection with Pasteurella multocida serogroup F strains originating from fowl cholera

Although Pasteurella multocida serogroup F has been described as an avian-adapted serogroup, it was recently found in rabbit nests in the Czech Republic. Therefore, the ability of 2 avian P. multocida serogroup F strains to induce disease in rabbits was investigated. Two groups of 18 Pasteurella-free rabbits were intranasally challenged with strains isolated from chickens and turkeys. Half of the animals in each challenge group were immunosuppressed using dexamethasone. All of the challenged rabbits exhibited clinical signs of peracute septicemic disease, ending with shock, and died or were euthanized in the terminal stages of the disease 1 to 2 d post-infection. Gross pathological changes included systemic vascular collapse and vascular leak syndrome. Hyperemia, hemorrhage, edema, inflammatory cell infiltrates, focal necrosis, and degenerative changes were observed histologically in parenchymatous organs. This is the first study directly demonstrating that avian P. multocida serogroup F strains are highly virulent in rabbits and that avian hosts cannot be excluded as a possible source of rabbit infection with serogroup F.     

Fatal coxiellosis in Swainson's Blue Mountain Rainbow Lorikeets (Trichoglossus haematodus moluccanus)

Three Swainson's Blue Mountain Rainbow Lorikeets (Trichoglossus haematodus moluccanus), ranging from 6 to 8 months of age, presented with lethargy, emaciation, and progressive neurologic signs. The first one died 24 hours after the onset of clinical signs, and the other two were euthanized 10 to 14 days after the onset of progressive neurologic disease. Clinical signs in these lorikeets included head pressing, hemiparesis, seizures, obtunded mentation, weakness, and lethargy. Two of the lorikeets had hepatomegaly, and one had splenomegaly on gross examination. Histopathology revealed disseminated microgranulomas in the liver, spleen, and brain, and lymphohistocytic perivascular encephalitis and cephalic vasculitis. Electron microscopic examination of macrophages in brain lesions revealed spherical to rod-shaped prokaryotic organisms with a trilaminar cell wall. Molecular analysis revealed a novel species of Coxiella. This is believed to be the first report of a Coxiella sp. causing disease in a lorikeet.     

Pathogenesis and transmissibility of highly (H7N1) and low (H7N9) pathogenic avian influenza virus infection in red-legged partridge (Alectoris rufa)

ABSTRACT: An experimental infection with highly pathogenic avian influenza virus (HPAIV) and low pathogenic avian influenza virus (LPAIV) was carried out in red-legged partridges (Alectoris rufa) in order to study clinical signs, gross and microscopic lesions, and viral distribution in tissues and viral shedding. Birds were infected with a HPAIV subtype H7N1 (A/Chicken/Italy/5093/1999) and a LPAIV subtype H7N9 (A/Anas crecca/Spain/1460/2008). Uninoculated birds were included as contacts in both groups. In HPAIV infected birds, the first clinical signs were observed at 3 dpi, and mortality started at 4 dpi, reaching 100% at 8 dpi. The presence of viral antigen in tissues and viral shedding were confirmed by immunohistochemistry and quantitative real time RT-PCR (qRRT-PCR), respectively, in all birds infected with HPAIV. However, neither clinical signs nor histopathological findings were observed in LPAIV infected partridges. In addition, only short-term viral shedding together with seroconversion was detected in some LPAIV inoculated animals. The present study demonstrates that the red-legged partridge is highly susceptible to the H7N1 HPAIV strain, causing severe disease, mortality and abundant viral shedding and thus contributing to the spread of a potential local outbreak of this virus. In contrast, our results concerning H7N9 LPAIV suggest that the red-legged partridge is not a reservoir species for this virus.     

A virulent mono-eukaryotic culture of Histomonas meleagridis is capable of inducing fatal histomonosis in different aged turkeys of both sexes, regardless of the infective dose

Histomonosis (syn. histomoniasis) is a parasitic disease which affects predominately turkeys but also other avian species. Concurrent with the ban of therapeutic and prophylactic substances, the disease, caused by the flagellated protozoon Histomonas meleagridis, is more frequently reported. Due to somewhat diverse results reported in the past, a well-characterized culture was used in the present study to investigate the possible influence of certain parameters on the outcome of the disease. For this study, turkeys were infected with different doses of the mono-eukaryotic culture Histomonas meleagridis/Turkey/Austria/2922-C6/04 using birds of both sexes at various ages. All study groups consisted of 14 birds, of which 10 birds were directly infected via the cloacal route and four birds were kept as in-contact birds. This scheme was used to investigate the pathogenicity of the cloned isolate in 1-day-old and 14-day-old turkeys. In 8-week-old turkeys, only eight birds out of 12 were infected. When 1-day-old and 8-week-old turkeys were infected with 10(4) histomonads per bird, all turkeys died between 11 and 21 days postinfection or had to be euthanatized due to their poor condition. In a group of 14 poults, infective doses of either 10 histomonads (100 histomonads among 10 birds) or 10(3) histomonads per bird had hardly any influence on the first notification of clinical signs. However, even though the onset of clinical signs and mortality was delayed with the lower dose, none of the birds survived the infection. As a consequence, no differences were noticed between male and female turkeys using the mono-eukaryotic culture of Histomonas meleagrigis/Turkey/Austria/2922-C6/04 in the current experimental setting.     

Pacheco's parrot disease in macaws of the Lisbon's Zoological Garden. Description of an outbreak, diagnosis and management, including vaccination

The Lisbon's Zoological Garden, Portugal, has maintained for many years a large collection of psittacine birds without any serious health problems. Unexpectedly, in April 1999, a total of nine macaws died after a short period of illness. Clinical signs consisted mainly of anorexia, ruffled feathers and yellowish droppings. A herpesvirus was isolated from brain, trachea, lung, liver, spleen, kidney and intestine of each of the examined dead birds, confirming that all animals succumbed during viraemia. Serotyping of the isolate in cross neutralization tests with reference sera prove that the outbreak was caused by serotype 3 of Pacheco's parrot disease herpesviruses. An autogenous, formalin-inactivated vaccine with adjuvant (aluminium hydroxid gel) was prepared from one of the isolates and injected intramuscularly 14 days and six weeks after the onset of mortality in an attempt to protect the remaining psittacine birds in the zoo from the disease. The autogenous vaccine was well tolerated and was able to rapidly stop virus spread and morbidity and mortality among the psittacine birds. Follow-up studies demonstrate that all nine blood samples from vaccinated birds obtained nine month' after the second vaccination contain neutralizing antibodies. Twenty five month' after vaccination two out of four serum samples were still antibody positive. No herpesvirus was isolated from faecal samples nine and twenty five months after the onset of the outbreak. These data prove that the autogenous vaccine played a major role in containing a severe outbreak of Pacheco's parrot disease in a large collection of psittacine birds.     

Preliminary results of an anticircumsporozoite DNA vaccine trial for protection against avian malaria in captive African black-footed penguins (Spheniscus demersus).

Captive juvenile African black-footed penguins (Spheniscus demersus) housed in an outdoor enclosure at the Baltimore Zoo have an average 50% mortality from avian malarial (Plasmodium sp.) infection each year without intense monitoring for disease and chemotherapeutic intervention. During the 1996 malaria transmission season, the safety and efficacy of an anti-circumsporozoite (CSP) DNA vaccine encoding the Plasmodium gallinaceum CSP protein against P. relictum were studied. The goal was to reduce clinical disease and death without initiating sterile immunity after release into an area with stable, endemic avian malaria. The birds were monitored for adverse clinical signs associated with vaccination, the stimulation of an anti-CSP antibody response, and protection afforded by the vaccine. The presence of P. relictum in trapped culicine mosquitoes within the penguin enclosure was monitored to assess parasite pressure. Among the vaccinated penguins, the parasitemia rate dropped from approximately 50% to approximately 17% despite intense parasite pressure, as determined by mosquito infection rate. During the year of the vaccine trial, no mortalities due to malaria occurred and no undesirable vaccination side effects occurred. This is the first trial of an antimalarial vaccine in a captive penguin colony.     

Disseminated histoplasmosis in an African pygmy hedgehog

CASE DESCRIPTION: A 2-year-old captive-bred sexually intact female African pygmy hedgehog (Atelerix albiventris) was evaluated because of vague signs of illness including inappetence, weakness, lethargy, and weight loss over a 20-day period. CLINICAL FINDINGS: Abnormalities detected via initial clinicopathologic analyses included anemia, thrombocytopenia, leukopenia, hypoproteinemia, and hypoglycemia. Results of a fecal flotation test were negative. Three weeks after the initial evaluation, splenomegaly was detected via palpation and ultrasonography. TREATMENT AND OUTCOME: The hedgehog was treated with broad-spectrum antibacterial agents, resulting in an initially favorable response. Fenbendazole was also administered against possible occult parasitic infestation. After 3 weeks of illness, the hedgehog's condition had worsened and supportive care and administration of additional antibacterial agents were instituted. The hedgehog died, and pathologic examinations revealed severe splenomegaly; granulomatous infiltrates were evident in multiple organs, and Histoplasma capsulatum yeasts were detected intralesionally. CLINICAL RELEVANCE: Histoplasmosis can develop in a wide range of mammalian species. African pygmy hedgehogs are becoming increasingly popular as exotic pets, and vague signs of illness and splenomegaly are often attributed to hemolymphatic malignancies, which are somewhat common in this species. Practitioners should be aware that similar clinical signs may be associated with histoplasmosis in these animals. Although the hedgehog of this report was confined indoors, it originated from an area where histoplasmosis was endemic; this indicates that the disease should be included as a differential diagnosis for hedgehogs that develop vague signs of illness and are known to originate from such geographic regions.     

Adverse reactions suggestive of type III hypersensitivity in six healthy dogs given human albumin

CASE DESCRIPTION:6 healthy dogs given human albumin solution as part of a study were examined following development of an immediate hypersensitivity reaction (1 dog) and signs suggestive of a type III hypersensitivity reaction (all 6 dogs). CLINICAL FINDINGS: All 6 dogs were healthy prior to administration of human albumin solution. One dog developed signs of an immediate hypersensitivity reaction, characterized by vomiting and facial edema, during administration of human albumin solution. All 6 dogs developed signs of a delayed adverse reaction 5 to 13 days after administration of human albumin solution. Initial clinical signs included lethargy, lameness, edema, cutaneous lesions indicative of vasculitis, vomiting, and inappetance. TREATMENT AND OUTCOME: In the dog with signs of immediate hypersensitivity, signs resolved after administration of human albumin solution was discontinued and diphenhydramine was administered. Supportive treatment was provided after dogs developed signs of a delayed adverse reaction. Four dogs recovered, but 2 dogs died despite treatment. All 6 dogs were found to have antihuman albumin antibodies. There was no evidence of contamination of the human albumin solution. CLINICAL RELEVANCE: Findings suggest that administration of human albumin solution in healthy dogs with normal serum albumin concentrations may result in signs of a type III hypersensitivity reaction.     

Successful treatment and polymerase chain reaction (PCR) confirmation of Tyzzer's disease in a foal and clinical and pathologic characteristics of 6 additional foals (1986-2005)

BACKGROUND: Tyzzer's disease is a rapidly progressive and highly fatal hepatitis of foals caused by Clostridium piliforme. Survival of a confirmed case has not been reported previously. HYPOTHESIS: Successful therapy of C. piliforme infection in foals is possible. Polymerase chain reaction (PCR) can be used to diagnose Tyzzer's disease antemortem or postmortem. ANIMALS: Seven foals were included in the study. METHODS: Retrospective study was made to evaluate the clinical and pathologic characteristics of foals with Tyzzer's disease. Medical records of the Veterinary Medical Teaching Hospital at University of California Davis were reviewed. Foals <3 months old were included in the study if typical clinical signs were present and histologic examination identified multifocal coagulative necrosis and hepatitis with intracytoplasmic filamentous bacilli, consistent with C. piliforme. A real-time TaqMan assay was developed to detect C. piliforme gene sequences in liver tissue from affected foals. RESULTS: Median survival time from onset of disease in nonsurviving foals was 30 hours (mean 34.5 +/- 20.1; range, 16-62 hours). Common clinical findings included lethargy, recumbency, seizures, and fever. Laboratory findings included metabolic acidosis, hypoglycemia and increased activity of hepatobiliary enzymes. Treatment consisted of IV fluids, antimicrobial and antiinflammatory drugs, and parenteral nutrition. One filly survived, whereas 6 died. Postmortem examination of the 6 foals that died disclosed hepatomegaly with multifocal necrosis. Liver tissue from 4 foals was positive for C. piliforme gene sequences using PCR. CONCLUSIONS AND CLINICAL IMPORTANCE: Although the mortality rate of Tyzzer's disease is high, successful outcome is possible if intensive care is initiated promptly. PCR can be used for early and specific diagnosis.     

Severe renal oxalosis in five young Beefmaster calves.

Severe renal oxalosis was diagnosed in 4 male and 1 female purebred Beefmaster calves from herds in southeastern and northwestern United States. Clinical signs included weakness, anorexia, lethargy, alopecia, dehydration, and diarrhea. Results of serum biochemical analysis for 2 calves were consistent with end-stage renal disease. Calves died 2 days to 6 weeks after birth. At necropsy, renal calyces were dilated and contained pale yellow granular calculi. Histologically, there was renal interstitial fibrosis, and cortical and medullary tubules were distended with calcium oxalate crystals. Oxalate crystals were also in the tracheal glands of 1 calf. Severe renal oxalosis in young purebred calves, on widely varied diets, with no known exposure to exogenous oxalates is suggestive of an inherited metabolic defect resulting in primary hyperoxaluria.